An advertisement revealing how alcohol absorbs into bloodstreams and can cause cancer is the most effective alcohol education ad internationally, a Cancer Council Victoria suggests. 
 
 ‘Spread’, created by The Brand Agency in 2010 for the Western Australia Alcohol and Drug Office, shows how drinking too much alcohol could heighten risks of cell mutations and cause cancer. 
 
 Published in the British Medical Journal Open, the study compared 83 alcohol education advertisements around the world, with ‘Spread’ reported as the most likely to motivate drinkers to reduce alcohol consumption. 
 
 The study involved 2,174 adults who regularly consume alcohol. The study subjects were shown three randomly selected ads from the pool of options before reporting the extent to which they felt motivated to reduce drinking following the viewing. 
 
 Each advertisement was scored on a five-point scale, with one being lowest and five being highest motivation. 
 
 ‘Spread’ received a score of 3.77, performing best among male and females, all ages, as well as low and high-risk drinkers. 
 
 Todd Harper, Cancer Council Victoria’s CEO said the research shows how campaigns can be used to help inform the public of the long-term consequences of alcohol consumption. 
 
 “We’ve seen how effective campaigns around drink driving and short-term harms such as injury or violence have been in terms of changing our drinking habits, but in Victoria and the majority of the rest of Australia, we rarely see the long-term health effects of alcohol portrayed on our screens,” he said. 
 
 “This research highlights how effective a campaign like this could be in terms of motivating people to better understand the risks of alcohol consumption. 
 
 “These findings should now be used to plan campaigns that empower the community with knowledge about the harms of alcohol, so they can reduce their cancer risk.” 
 
 The study was conducted by the Cancer Council’s Centre for Behavioural Research in Cancer and funded by the National Health and Medical Research Council. 
 
 Cancer Council Victoria hopes to use the advertisement in a campaign later this year. 
 
 Nine’s Today Show Extra this morning built on Harper’s comments, discussing whether alcohol packaging could or should go in the same direction as cigarette advertising, following the study’s revelations. ||||| Known and Probable Human Carcinogens 
 
 Many people worry that substances or exposures in their environment may cause cancer. As part of the American Cancer Society’s role in informing and educating people about cancer and its possible causes, this document provides lists of substances and exposures that are known or suspected to cause cancer. The lists below have been developed by two highly respected agencies – the International Agency for Research on Cancer (IARC) and the US National Toxicology Program (NTP). Some related information is included on how these and other agencies and groups test and classify possible carcinogens. 
 
 The American Cancer Society does not keep detailed information on each of the exposures on these lists. If you are looking for more in-depth information on a particular item on these lists, please refer to the agencies in the “Additional resources” section. 
 
 What is a carcinogen? 
 
 Cancer is caused by changes in a cell’s DNA – its genetic “blueprint.” Some of these changes may be inherited from our parents. Others may be caused by outside exposures, which are often referred to as environmental factors. Environmental factors can include a wide range of exposures, such as: 
 
 Lifestyle factors (nutrition, tobacco use, physical activity, etc.) 
 
 Naturally occurring exposures (ultraviolet light, radon gas, infectious agents, etc.) 
 
 Medical treatments (radiation and medicines including chemotherapy, hormone drugs, drugs that suppress the immune system, etc.) 
 
 Workplace exposures 
 
 Household exposures 
 
 Pollution 
 
 Substances and exposures that can lead to cancer are called carcinogens. Some carcinogens do not affect DNA directly, but lead to cancer in other ways. For example, they may cause cells to divide at a faster than normal rate, which could increase the chances that DNA changes will occur. 
 
 Carcinogens do not cause cancer in every case, all the time. Substances labeled as carcinogens may have different levels of cancer-causing potential. Some may cause cancer only after prolonged, high levels of exposure. And for any particular person, the risk of developing cancer depends on many factors, including how they are exposed to a carcinogen, the length and intensity of the exposure, and the person's genetic makeup. 
 
 How do researchers determine if something is a carcinogen? 
 
 Testing to see if something can cause cancer is often difficult. It is not ethical to test a substance by exposing people to it and seeing if they get cancer from it. That’s why scientists must use other types of tests, which may not always give clear answers. 
 
 Lab studies 
 
 Scientists get much of their data about whether something might cause cancer from lab studies in cell cultures and animals. There are far too many substances (both natural and man-made) to test each one in lab animals, so scientists use what is already known about chemical structures, results from other types of lab tests, the extent of human exposure, and other factors to select chemicals for testing. For example, they can often get an idea about whether a substance might cause a problem by comparing it to similar chemicals that have already been studied. 
 
 Although lab studies alone can't always predict if a substance will cause cancer in people, virtually all known human carcinogens that have been adequately tested also cause cancer in lab animals. In many cases, carcinogens are first found to cause cancer in lab animals and are later found to cause cancer in people. 
 
 Most studies of potential carcinogens expose the lab animals to doses that are much higher than common human exposures. This is so that cancer risk can be detected in relatively small groups of animals. It is not always clear if the results from animal studies will be the same for people as they are normally exposed to a substance. For example, the effects seen in lab studies with very high doses of a substance may not be the same at much lower doses, or the effects of a substance when it is inhaled may not be the same as if it is applied to the skin. Also, the bodies of lab animals and humans don't always process substances in the same way. 
 
 But for safety reasons, it is usually assumed that exposures that cause cancer at larger doses in animals may also cause cancer in people. It isn't always possible to know how the exposure dose might affect risk, but it is reasonable for public health purposes to assume that lowering human exposure will reduce risk. 
 
 Studies in people 
 
 Another important way to identify carcinogens is through epidemiologic studies, which look at human populations to determine which factors might be linked to cancer. These studies also provide useful information, but they have their limits. Humans do not live in a controlled environment. People are exposed to many substances at any given time, including those they encounter at work, school, or home; in the food they eat; and in the air they breathe. It's very unlikely they know exactly what they've been exposed to or that they would be able to remember all of their exposures if asked by a researcher. And there are usually many years (often decades) between exposure to a carcinogen and the development of cancer. Therefore, it can be very hard to definitely link any particular exposure to cancer. 
 
 By combining data from both types of studies, scientists do their best to make an educated assessment of a substance's cancer-causing ability. When the evidence is conclusive, the substance is labeled as a carcinogen. When the available evidence is compelling but not felt to be conclusive, the substance may be considered to be a probable carcinogen. But in some cases there simply isn't enough information to be certain one way or the other. 
 
 Who determines how carcinogens are classified? 
 
 Several national and international agencies are responsible for determining the cancer-causing potential of different substances. 
 
 International Agency for Research on Cancer 
 
 The International Agency for Research on Cancer (IARC) is part of the World Health Organization (WHO). One of its major goals is to identify causes of cancer. The most widely used system for classifying carcinogens comes from the IARC. In the past 30 years, the IARC has evaluated the cancer-causing potential of more than 900 likely candidates, placing them into one of the following groups: 
 
 Group 1: Carcinogenic to humans 
 
 Group 2A: Probably carcinogenic to humans 
 
 Group 2B: Possibly carcinogenic to humans 
 
 Group 3: Unclassifiable as to carcinogenicity in humans 
 
 Group 4: Probably not carcinogenic to humans 
 
 Perhaps not surprisingly, based on how hard it can be to test these candidate carcinogens, most are listed as being of probable, possible, or unknown risk. Only a little over 100 are classified as “carcinogenic to humans.” 
 
 National Toxicology Program 
 
 The National Toxicology Program (NTP) is formed from parts of several different US government agencies, including the National Institutes of Health (NIH), the Centers for Disease Control and Prevention (CDC), and the Food and Drug Administration (FDA). The NTP updates its Report on Carcinogens (RoC) every few years. 
 
 The Report on Carcinogens identifies 2 groups of agents: 
 
 “Known to be human carcinogens” 
 
 “Reasonably anticipated to be human carcinogens” 
 
 The current version of the RoC lists about 250 substances and exposures. Unlike the IARC’s list, the RoC does not list substances that have been studied and found not to be carcinogens. 
 
 Environmental Protection Agency 
 
 The US Environmental Protection Agency (EPA) maintains the Integrated Risk Information System (IRIS), an electronic database that contains information on human health effects from exposure to certain substances in the environment. The EPA uses a rating system similar to that of IARC when describing the cancer-causing potential of a substance: 
 
 Group A: Carcinogenic to humans 
 
 Group B: Likely to be carcinogenic to humans 
 
 Group C: Suggestive evidence of carcinogenic potential 
 
 Group D: Inadequate information to assess carcinogenic potential 
 
 Group E: Not likely to be carcinogenic to humans 
 
 Other agencies and groups 
 
 Other federal agencies, such as the CDC’s National Institute for Occupational Safety and Health (NIOSH), the Food and Drug Administration (FDA), and the National Cancer Institute (NCI) may comment on whether a substance or exposure may cause cancer and/or what levels of exposure to a particular substance might be considered acceptable. 
 
 Some state agencies also keep lists of known or probable carcinogens. For example, the California Environmental Protection Agency (CalEPA) maintains a list of “chemicals known to the state to cause cancer or reproductive toxicity.” (Much of this list is based on the IARC and NTP lists below.) 
 
 The American Cancer Society’s role 
 
 The American Cancer Society (ACS) contributes in many ways to evaluating how environmental factors affect a person's likelihood of developing cancer, including: 
 
 Conducting epidemiologic research on the causes of cancer 
 
 Funding laboratory and epidemiologic research at universities and other institutions that study environmental causes of cancer 
 
 Advocating for environmental health on local, state, and federal levels 
 
 Informing the public about environmental factors that affect cancer risk and how to decrease their risk of developing cancer 
 
 In most cases, the ACS does not directly evaluate whether a certain substance or exposure causes cancer. Instead, the ACS looks to national and international organizations such as the NTP and IARC, whose mission is to evaluate environmental cancer risks based on evidence from laboratory and human research studies. 
 
 Some important points about the IARC and NTP lists here 
 
 The IARC and NTP act independently but have studied many of the same agents, so many known or suspected carcinogens appear on both lists. But because an agent appears on one and not on the other does not necessarily mean there is a controversy, as one agency may not have evaluated it. 
 
 Unfortunately, many of the substances and exposures on the lists below can often go by different names. This can make it hard to find a particular substance on one or both of these lists, which are in alphabetical order and may not always use the most common term. 
 
 These lists include only those agents that have been evaluated by the agencies. These agencies tend to focus on substances and exposures most likely to cause cancer, but there are many others that have not been studied fully yet. 
 
 Most of the agents on the lists have been linked only with certain kinds of cancer, not all types. For more detailed information, refer to the specific monographs or reports published by the agencies (available on their websites). 
 
 The lists describe the level of evidence that something can cause cancer, not how likely it is that something will cause cancer in any particular person. For example, IARC considers there to be strong evidence that both tobacco smoking and eating processed meat can cause cancer, so both are listed as “carcinogenic to humans.” But smoking is much more likely to cause cancer than eating processed meat, even though both are in the same category. 
 
 Carcinogens do not cause cancer at all times, under all circumstances. Some may only be carcinogenic if a person is exposed in a certain way (for example, swallowing it as opposed to touching it). Some may only cause cancer in people who have a certain genetic makeup. Some of these agents may lead to cancer after only a very small exposure, while others might require intense exposure over many years. Again, you should refer to the agencies’ reports for specifics. 
 
 Even if a substance or exposure is known or suspected to cause cancer, this does not necessarily mean that it can or should be avoided at all costs. For example, estrogen is a known carcinogen that occurs naturally in the body. Exposure to ultraviolet (UV) radiation from sunlight is also known to cause cancer, but it’s not practical (or advisable) to completely avoid the sun. These lists also include many commonly used medicines, particularly some hormones and drugs used to treat cancer. For example, tamoxifen increases the risk of certain kinds of uterine cancer but can be very useful in treating some breast cancers, which may be more important for some women. If you have questions about a medicine that appears on one of these lists, be sure to ask your doctor. 
 
 Looking at the list below can tell you whether or not something may increase your risk of cancer, but it is important to try to get an idea of how much it might increase your risk. It is also important to know what your risk is to begin with. Many factors can enter into this, including your age, gender, family history, and lifestyle factors (tobacco and alcohol use, weight, diet, physical activity level, etc.). As noted above, the type and extent of exposure to a substance may also play a role. You should consider the actual amount of increased risk when deciding if you should limit or avoid an exposure. 
 
 Known human carcinogens 
 
 International Agency for Research on Cancer 
 
 Group 1: Carcinogenic to humans 
 
 Acetaldehyde (from consuming alcoholic beverages) 
 
 Acheson process, occupational exposure associated with 
 
 Acid mists, strong inorganic 
 
 Aflatoxins 
 
 Alcoholic beverages 
 
 Aluminum production 
 
 4-Aminobiphenyl 
 
 Areca nut 
 
 Aristolochic acid (and plants containing it) 
 
 Arsenic and inorganic arsenic compounds 
 
 Asbestos (all forms) and mineral substances (such as talc or vermiculite) that contain asbestos 
 
 Auramine production 
 
 Azathioprine 
 
 Benzene 
 
 Benzidine and dyes metabolized to benzidine 
 
 Benzo[a]pyrene 
 
 Beryllium and beryllium compounds 
 
 Betel quid, with or without tobacco 
 
 Bis(chloromethyl)ether and chloromethyl methyl ether (technical-grade) 
 
 Busulfan 
 
 1,3-Butadiene 
 
 Cadmium and cadmium compounds 
 
 Chlorambucil 
 
 Chlornaphazine 
 
 Chromium (VI) compounds 
 
 Clonorchis sinensis (infection with), also known as the Chinese liver fluke 
 
 (infection with), also known as the Chinese liver fluke Coal, indoor emissions from household combustion 
 
 Coal gasification 
 
 Coal-tar distillation 
 
 Coal-tar pitch 
 
 Coke production 
 
 Cyclophosphamide 
 
 Cyclosporine 
 
 1,2-Dichloropropane 
 
 Diethylstilbestrol 
 
 Engine exhaust, diesel 
 
 Epstein-Barr virus (infection with) 
 
 Erionite 
 
 Estrogen postmenopausal therapy 
 
 Estrogen-progestogen postmenopausal therapy (combined) 
 
 Estrogen-progestogen oral contraceptives (combined) (Note: There is also convincing evidence in humans that these agents confer a protective effect against cancer in the endometrium and ovary) 
 
 Ethanol in alcoholic beverages 
 
 Ethylene oxide 
 
 Etoposide 
 
 Etoposide in combination with cisplatin and bleomycin 
 
 Fission products, including strontium-90 
 
 Fluoro-edenite fibrous amphibole 
 
 Formaldehyde 
 
 Haematite mining (underground) 
 
 Helicobacter pylori (infection with) 
 
 (infection with) Hepatitis B virus (chronic infection with) 
 
 Hepatitis C virus (chronic infection with) 
 
 Human immunodeficiency virus type 1 (HIV-1) (infection with) 
 
 Human papilloma virus (HPV) types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59 (infection with) (Note: The HPV types that have been classified as carcinogenic to humans can differ by an order of magnitude in risk for cervical cancer) 
 
 Human T-cell lymphotropic virus type I (HTLV-1) (infection with) 
 
 Ionizing radiation (all types) 
 
 Iron and steel founding (workplace exposure) 
 
 Isopropyl alcohol manufacture using strong acids 
 
 Kaposi sarcoma herpesvirus (KSHV), also known as human herpesvirus 8 (HHV-8) (infection with) 
 
 Leather dust 
 
 Lindane 
 
 Magenta production 
 
 Melphalan 
 
 Methoxsalen (8-methoxypsoralen) plus ultraviolet A radiation, also known as PUVA 
 
 4,4'-Methylenebis(chloroaniline) (MOCA) 
 
 Mineral oils, untreated or mildly treated 
 
 MOPP and other combined chemotherapy including alkylating agents 
 
 2-Naphthylamine 
 
 Neutron radiation 
 
 Nickel compounds 
 
 N'-Nitrosonornicotine (NNN) and 4-(N-Nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK) 
 
 Opisthorchis viverrini (infection with), also known as the Southeast Asian liver fluke 
 
 (infection with), also known as the Southeast Asian liver fluke Outdoor air pollution (and the particulate matter in it) 
 
 Painter (workplace exposure as a) 
 
 3,4,5,3',4'-Pentachlorobiphenyl (PCB-126) 
 
 2,3,4,7,8-Pentachlorodibenzofuran 
 
 Phenacetin (and mixtures containing it) 
 
 Phosphorus-32, as phosphate 
 
 Plutonium 
 
 Polychlorinated biphenyls (PCBs), dioxin-like, with a Toxicity Equivalency Factor according to WHO (PCBs 77, 81, 105, 114, 118, 123, 126, 156, 157, 167, 169, 189) 
 
 Processed meat (consumption of) 
 
 Radioiodines, including iodine-131 
 
 Radionuclides, alpha-particle-emitting, internally deposited (Note: Specific radionuclides for which there is sufficient evidence for carcinogenicity to humans are also listed individually as Group 1 agents) 
 
 Radionuclides, beta-particle-emitting, internally deposited (Note: Specific radionuclides for which there is sufficient evidence for carcinogenicity to humans are also listed individually as Group 1 agents) 
 
 Radium-224 and its decay products 
 
 Radium-226 and its decay products 
 
 Radium-228 and its decay products 
 
 Radon-222 and its decay products 
 
 Rubber manufacturing industry 
 
 Salted fish (Chinese-style) 
 
 Schistosoma haematobium (infection with) 
 
 (infection with) Semustine (methyl-CCNU) 
 
 Shale oils 
 
 Silica dust, crystalline, in the form of quartz or cristobalite 
 
 Solar radiation 
 
 Soot (as found in workplace exposure of chimney sweeps) 
 
 Sulfur mustard 
 
 Tamoxifen (Note: There is also conclusive evidence that tamoxifen reduces the risk of contralateral breast cancer in breast cancer patients) 
 
 2,3,7,8-Tetrachlorodibenzo-para-dioxin 
 
 Thiotepa 
 
 Thorium-232 and its decay products 
 
 Tobacco, smokeless 
 
 Tobacco smoke, secondhand 
 
 Tobacco smoking 
 
 ortho-Toluidine 
 
 Treosulfan 
 
 Trichloroethylene 
 
 Ultraviolet (UV) radiation, including UVA, UVB, and UVC rays 
 
 Ultraviolet-emitting tanning devices 
 
 Vinyl chloride 
 
 Wood dust 
 
 X- and Gamma-radiation 
 
 National Toxicology Program 14th Report on Carcinogens 
 
 “Known to be human carcinogens” 
 
 Aflatoxins 
 
 Alcoholic beverage consumption 
 
 4-Aminobiphenyl 
 
 Analgesic mixtures containing phenacetin 
 
 Aristolochic acids 
 
 Arsenic and inorganic arsenic compounds 
 
 Asbestos 
 
 Azathioprine 
 
 Benzene 
 
 Benzidine 
 
 Beryllium and beryllium compounds 
 
 Bis(chloromethyl) ether and technical-grade chloromethyl methyl ether 
 
 1,3-Butadiene 
 
 1,4-Butanediol dimethylsulfonate (also known as busulfan) 
 
 Cadmium and cadmium compounds 
 
 Chlorambucil 
 
 1-(2-Chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea (MeCCNU) 
 
 Chromium hexavalent compounds 
 
 Coal tar pitches 
 
 Coal tars 
 
 Coke oven emissions 
 
 Cyclophosphamide 
 
 Cyclosporin A 
 
 Diethylstilbestrol (DES) 
 
 Dyes metabolized to benzidine 
 
 Epstein-Barr virus (EBV) 
 
 Erionite 
 
 Estrogens, steroidal 
 
 Ethylene oxide 
 
 Formaldehyde 
 
 Hepatitis B virus 
 
 Hepatitis C virus 
 
 Human immunodeficiency virus type 1 (HIV-1) 
 
 Human papilloma viruses: some genital-mucosal types 
 
 Human T-cell lymphotropic virus type 1 (HTLV-1) 
 
 Kaposi sarcoma-associated herpesvirus (KSHV) (also know as human herpesvirus 8, or HHV-8) 
 
 Melphalan 
 
 Merkel cell polyomavirus (MCV) 
 
 Methoxsalen with ultraviolet A therapy (PUVA) 
 
 Mineral oils (untreated and mildly treated) 
 
 Mustard gas 
 
 2-Naphthylamine 
 
 Neutrons 
 
 Nickel compounds 
 
 Oral tobacco products 
 
 Radon 
 
 Silica, crystalline (respirable size) 
 
 Solar radiation 
 
 Soots 
 
 Strong inorganic acid mists containing sulfuric acid 
 
 Sunlamps or sunbeds, exposure to 
 
 Tamoxifen 
 
 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD); "dioxin" 
 
 Thiotepa 
 
 Thorium dioxide 
 
 Tobacco smoke, environmental 
 
 Tobacco, smokeless 
 
 Tobacco smoking 
 
 o‑Toluidine 
 
 Trichloroethylene (TCE) 
 
 Vinyl chloride 
 
 Ultraviolet (UV) radiation, broad spectrum 
 
 Wood dust 
 
 X-radiation and gamma radiation 
 
 Probable carcinogens 
 
 International Agency for Research on Cancer 
 
 Group 2A: Probably carcinogenic to humans 
 
 Acrylamide 
 
 Adriamycin (doxorubicin) 
 
 Androgenic (anabolic) steroids 
 
 Art glass, glass containers, and press ware (manufacture of) 
 
 Azacitidine 
 
 Biomass fuel (primarily wood), emissions from household combustion 
 
 Bischloroethyl nitrosourea (BCNU), also known as carmustine 
 
 Captafol 
 
 Carbon electrode manufacture 
 
 Chloral 
 
 Chloral hydrate 
 
 Chloramphenicol 
 
 alpha-Chlorinated toluenes (benzal chloride, benzotrichloride, benzyl chloride) and benzoyl chloride (combined exposures) 
 
 1-(2-Chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU) 
 
 4-Chloro-ortho-toluidine 
 
 Chlorozotocin 
 
 Cisplatin 
 
 Cobalt metal with tungsten carbide 
 
 Creosotes 
 
 Cyclopenta[cd]pyrene 
 
 DDT (4,4'-Dichlorodiphenyltrichloroethane) 
 
 Diazinon 
 
 Dibenz[a,j]acridine 
 
 Dibenz[a,h]anthracene 
 
 Dibenzo[a,l]pyrene 
 
 Dichloromethane (methylene chloride) 
 
 Diethyl sulfate 
 
 Dimethylcarbamoyl chloride 
 
 1,2-Dimethylhydrazine 
 
 Dimethyl sulfate 
 
 Epichlorohydrin 
 
 Ethyl carbamate (urethane) 
 
 Ethylene dibromide 
 
 N-Ethyl-N-nitrosourea 
 
 Frying, emissions from high-temperature 
 
 Glycidol 
 
 Glyphosate 
 
 Hairdresser or barber (workplace exposure as) 
 
 Human papillomavirus (HPV) type 68 (infection with) 
 
 Indium phosphide 
 
 IQ (2-Amino-3-methylimidazo[4,5-f]quinoline) 
 
 Lead compounds, inorganic 
 
 Malaria (caused by infection with Plasmodium falciparum ) 
 
 ) Malathion 
 
 Merkel cell polyomavirus (MCV) 
 
 5-Methoxypsoralen 
 
 Methyl methanesulfonate 
 
 N-Methyl-N´-nitro-N-nitrosoguanidine (MNNG) 
 
 N-Methyl-N-nitrosourea 
 
 Nitrate or nitrite (ingested) under conditions that result in endogenous nitrosation 
 
 6-Nitrochrysene 
 
 Nitrogen mustard 
 
 1-Nitropyrene 
 
 N-Nitrosodiethylamine 
 
 N-Nitrosodimethylamine 
 
 2-Nitrotoluene 
 
 Non-arsenical insecticides (workplace exposures in spraying and application of) 
 
 Petroleum refining (workplace exposures in) 
 
 Pioglitazone 
 
 Polybrominated biphenyls (PBBs) 
 
 Procarbazine hydrochloride 
 
 1,3-Propane sultone 
 
 Red meat (consumption of) 
 
 Shiftwork that involves circadian disruption 
 
 Silicon carbide whiskers 
 
 Styrene-7,8-oxide 
 
 Teniposide 
 
 Tetrachloroethylene (perchloroethylene) 
 
 Tetrafluoroethylene 
 
 Trichloroethylene 
 
 1,2,3-Trichloropropane 
 
 Tris(2,3-dibromopropyl) phosphate 
 
 Very hot beverages (above 65 degrees Celsius) 
 
 Vinyl bromide (Note: For practical purposes, vinyl bromide should be considered to act similarly to the human carcinogen vinyl chloride.) 
 
 Vinyl fluoride (Note: For practical purposes, vinyl fluoride should be considered to act similarly to the human carcinogen vinyl chloride.) 
 
 National Toxicology Program 14th Report on Carcinogens 
 
 “Reasonably anticipated to be human carcinogens” ||||| The interactive transcript could not be loaded. 
 
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 This feature is not available right now. Please try again later. ||||| Given limited resources, it is crucial that funding is devoted to messages with the greatest likelihood of promoting behaviour change. Perceived effectiveness measures are often used to pretest the likely success of potential campaign messages, with several studies on tobacco control messages establishing their predictive validity for increased intentions to quit, 39 more thoughts about quitting 40 and behaviour change. 41 , 42 A recent review defined perceived effectiveness as “the extent to which a message recipient believes that a health message will affect him or her personally in terms of the particular message objectives”. 43 As a step towards identifying specific advertisements (ads) and message features that may hold the most promise for population-wide behaviour change, the primary aim of the study was to examine the comparative perceived effectiveness of a large pool of alcohol harm reduction ads with variable features, using a measure of the extent to which adult weekly drinkers felt motivated by them to reduce the amount of alcohol they drink. A secondary aim was to determine the top-ranked ads for drinkers overall compared with high-risk drinkers and other key demographic subgroups, providing a preliminary test of the merit of a ‘common denominator’ approach. A third aim was to identify the informational content, executional style and other message features associated with highly ranked ads. 
 
 Several recent successful examples of alcohol harm reduction advertising also suggest that a general population, rather than targeted audience, approach may hold promise. 33 , 34 Conceptualised more generally, mass media campaigns can either target messages to particular subgroups (typically high-risk individuals or key demographic groups) or use a whole-of-population approach. While targeting campaigns to subgroups holds logical appeal, others have noted that this approach also carries risks. A focus on particular high-risk population subgroups (such as young adults) can exempt people outside those groups (such as older adults) from heeding the message even though they may also be at risk, promoting a culture in which ‘our’ drinking is acceptable and ‘their’ drinking is problematic. 35 , 36 Relatedly, campaigns that are narrowly targeted miss the opportunity to change broader social norms by encouraging the wider population to reflect on their own behaviour and generating wider public debate that can build support for policy change. 36 , 37 Finally, narrowly targeted campaigns can be inefficient, requiring multiple messages for different groups which are expensive to develop and sustain. 36 As Hornik and colleagues have suggested, there may be merit in adopting a ‘common denominator’ approach, 36 , 38 where a single campaign is used to address beliefs that are commonly shared across many subgroups, thus serving multiple audiences at the same time. Such an approach also provides the opportunity to stimulate broader community discussion and normative change. 
 
 One means for achieving improved awareness could be through the delivery of mass media campaigns that warn the public of the negative consequences of alcohol use. Mass media campaigns have been successful for changing many health behaviours, 13 most notably in reducing tobacco use. 14 , 15 Yet aside from the success of campaigns to reduce drink driving 16 there is limited evidence to date that alcohol harm reduction campaigns—most of which have focussed on youth—are effective. 13 , 17 , 18 This limited success could be due to many factors, 13 including inadequate reach, frequency and duration, the lack of integration of public education with a sustained comprehensive approach involving other alcohol control policies including price controls 17 , 19 and the unrestricted volume of pro-drinking alcohol marketing which dwarfs sporadic educational efforts. 19 , 20 Integration of policy and public education efforts is typified in the successful whole-of-population approach in tobacco control that has changed social norms and reduced adult and youth smoking rates. 13 , 15 , 21–26 Evidence from tobacco control has also demonstrated that message attributes are more important than audience attributes in identifying effective campaigns, 14 , 27 with particular campaign messages—such as those promoting why people need to quit rather than how to quit and those that evoke negative emotion through graphic imagery or personal stories of serious harm—performing well across many population subgroups. 14 , 27–32 
 
 Alcohol use ranks among the top five risk factors for global disease burden, accounting for 5.5% of all disability adjusted life years lost. 1 About 70% of this alcohol burden is due to long-term harms such as cancer, cardiovascular disease, neuropsychiatric disorders and infectious disease, with the remainder due to short-term harms including unintentional and intentional injury. 2 In developed nations such as Australia, the UK, Ireland and the USA, population awareness of the range of harms from alcohol is limited. 3–8 For example, an Australian survey in 2014 found prompted awareness of the link between alcohol use and serious conditions to vary substantially, ranging from 80% for cirrhosis of the liver to only 15% for breast cancer. 9 Population surveys also show poor awareness of the levels of alcohol consumption associated with harm 10 and low-risk drinking guidelines. 9 , 11 Together, these findings indicate considerable scope for public education to improve awareness and understanding of alcohol-associated harms, with the broader goal of contributing to reductions in risky drinking. A keener awareness of harms is also critical if strong public support is to be expected for alcohol policy reform. 12 
 
 We used Fisher's exact tests to compare the characteristics of ads that were ranked in the top 15% (n=12 ads) with those ranked in the middle 70% (n=59) and the bottom 15% (n=12) within the overall sample. Fifteen per cent (n=12 ads) was chosen as the cut-off for the sets of top-ranked/bottom-ranked ads, as this provided a balance between having a sufficient number of ads to give stable estimates of the characteristics within each group while also limiting the number of ads to be considered by campaign planners wishing to select one of the top performing for use in their own jurisdiction. 
 
 Data were analysed using Stata/SE 14.2 (StataCorp. Stata Statistical Software: Release 14.2. College Station, TX: StataCorp LP; 2016). Multivariable linear regression models provided predicted means on the outcome of ‘motivated to reduce the amount of alcohol I drink’ for each ad, and assessed the statistical significance of differences between each ad and (1) the highest and then (2) the lowest ranked ad. One set of models was conducted for the overall sample (N=6522 unique ad ratings). Additional models were conducted stratified by demographic subgroups to examine differences in participants' ad rankings by age group (younger adults (n=3513 unique ad ratings) and older adults (n=3009)), sex (men (n=3123) and women (n=3999)) and drinking risk status (low risk (n=3327) and high risk (n=3195)). All models (overall sample and stratified models) employed data that were clustered by participant identification number to account for the same individual rating three ads using the cluster option in Stata, whereby robust SEs are used to allow for intragroup correlation. All models controlled for participant characteristics used for sample recruitment quotas and/or that were significantly associated with the outcome in bivariate models: NHMRC risk status (in four categories, as described above), perceived risk status, sex, tertiary education, parental status, age (continuous), familiarity with the ads, past 7 day alcohol consumption and alcohol identity. 
 
 Participants were asked one question about their perceived level of risk (adapted from 49 ): How would you describe the amount of alcohol you currently drink? Response options included: (1) ‘I definitely drink more than I should’; (2) ‘I probably drink more than I should’; (3) ‘The amount I drink is ok’ and (4) ‘I could drink more than I do’. Response options (1) and (2) were combined and classified as ‘at risk’; responses (3) and (4) were combined and classified as ‘low risk’. Two questions measured the importance of alcohol to the individual's self-identity (adapted from studies measuring the importance of tobacco smoking to self-identity 50 , 51 ): ‘drinking is part of who I am’ and ‘drinking is a part of my personality’. Responses were assessed using a five-point scale (1 ‘strongly disagree’—5 ‘strongly agree’), and were averaged to form a two-item measure of alcohol identity (α=0.904). 
 
 Baseline alcohol consumption was first assessed using the graduated quantity frequency measure, 10 a measure of average pattern of consumption based on how often in the past 12 months (every day, 5–6 days a week, 3–4 days a week, 1–2 days a week, 2–3 days a month, about 1 day a month, less often or never) participants had each of the following number of standard drinks in a day (20+, 11–19, 7–10, 5–6, 3–4, 1–2, <1 or no alcohol in a day). A standard drink in Australia is classified as 10g of alcohol, 47 and to aid accurate responses participants were provided with a visual guide of the number of standard drinks in common serving sizes of different alcoholic beverages. Applying the Australian National Health and Medical Research Council's (NHMRC) 2009 guidelines for low-risk drinking, 48 participants were classified as being at high risk of short-term harm if they reported having >4 drinks on any occasion at least once a month, and as being at high risk of long-term harm if they consumed >2 drinks per day on average. Participants were further classified into one of four categories: (1) low risk of harm in the short term and long term; (2) high risk of short-term harm but low risk of long-term harm; (3) low risk of short-term harm but high risk of long-term harm or (4) high risk of harm in the short term and long term. For comparative analyses, these categories were aggregated to compare those at low risk in the short term and long term (1; ‘low-risk drinkers’) with those at high risk in either or both the short term or long term (2, 3, 4; ‘high-risk drinkers’). Consumption was also measured using the seven-day timeline follow-back method, 48 to provide an estimate of recent consumption, whereby participants indicate how many alcoholic standard drinks they consumed each day of the past week, with each day and date labelled automatically in the online survey depending on the date of study completion. 
 
 After viewing each ad, participants completed a set of questions assessing their cognitive and emotional responses. In the current study, we focussed on the primary outcome of motivation to reduce the amount of alcohol consumed. This was determined by asking participants to indicate on a five-point scale (1 ‘strongly disagree’–5 ‘strongly agree’) the extent to which they ‘felt motivated to reduce the amount of alcohol I drink’ while watching the ad. Self-reported motivation to engage in behaviour change was part of the personalised perceived effectiveness scale validated as a predictor of subsequent behaviour change following exposure to tobacco control ads, 42 and is consistent with recent recommendations that the potential effectiveness of behaviour change messages be assessed by asking participants to report how likely it is that they will be personally affected in the way intended by the message. 43 There were moderate to strong positive correlations, ranging from 0.51 to 0.72, between this overarching general drinking reduction motivation and other more specific motivations, namely being motivated to: limit my drinking so I don't get drunk; behave responsibly when I drink; look after my friends and family when they are drinking; talk to a friend or family member about their drinking; limit my drinking when around children and teenagers; never supply alcohol to teenagers and (among parents) talk to my children about alcohol. These seven items were developed specifically for the study, and were intended to cover the full spectrum of behavioural objectives targeted by these ads, as identified in our recent content analysis. 45 The correlation results suggest that while different ads may seek to influence particular behaviours, if they are successful in doing so, they also elicit an overall motivation to reduce the amount of alcohol a person drinks. We therefore used this general reduced drinking motivational outcome as our primary ranking criterion; however, in a supplementary report, we present findings for all seven motivation items, to assist jurisdictions to select messages with the greatest potential to motivate adult drinkers to engage in a range of behaviours to reduce harm from alcohol. 46 
 
 Panel members were invited to participate via email with a web link to the study. Potential participants first completed questions assessing qualifying criteria and quotas. Prior to viewing ads, eligible participants were informed that some ads may be from different countries and that when watching each ad they should focus on its main message and imagery, rather than production quality or cultural differences such as accents. Participants were then shown their first ad twice, and asked to complete a series of ad ratings. This process was repeated for the remaining two ads randomly assigned to the participant. 
 
 While others have shown through modelling that stable ad ratings can be achieved with as few as 23 individuals rating each ad, 44 we set our target higher since random assignment of ads to participants meant some variability in the exact number of individuals rating each ad. We aimed for a sample size of 70 ratings per ad to facilitate comparisons of ad ratings within the key demographic subgroups of men/women (35 ratings per ad) and younger/older adults (35 ratings per ad). 
 
 The sample comprised 2174 18–64 year olds who reported consuming alcohol at least 1–2 days per week on average over the past 12 months (‘weekly drinkers’). 10 Participants were ineligible if they were pregnant or worked in health promotion, market research, advertising or the alcohol industry. Participants were recruited through an online panel that was accredited under the International Organization for Standardization's (ISO) standards for access panels in market, opinion and social research (AS ISO 26362). Quotas were applied to achieve approximately even numbers of men and women, and those aged 18–29 years (younger adults) and 30–64 years (older adults). 
 
 In an online study, Australian adult drinkers viewed and responded to three alcohol harm reduction television ads randomly selected from a pool of 83 ads. The study design minimised the possibility of order effects via random selection of ads from the pool and presenting them in a random order to each participant. The final rating obtained for each ad was aggregated across individuals and across orderings, and therefore controlled for order effects. Fieldwork was undertaken in October–November 2015. 
 
 While top-ranked ads did not differ in their use of graphic imagery, they were more likely than bottom-ranked ads to contain explicit portrayals of drinking (58% vs 8%, respectively) and were less likely to contain no portrayal of drinking than middle-ranked or bottom-ranked ads (0% vs 25% and 75%, respectively). Finally, a significantly higher proportion of top-ranked ads targeted a general adult audience (83%), whereas middle-ranked (46%) and bottom-ranked ads (58%) were more likely to specifically target young adults ( table 4 ). 
 
 The distribution of ads differed by emotional tone, with 50% of bottom-ranked ads having a positive tone compared with none of the top-ranked ads. Conversely, 92% of top-ranked ads had a negative tone compared with 50% of bottom-ranked ads, although this difference did not reach statistical significance (p=.085). In terms of execution, top-ranked ads were less likely to feature a dramatisation communication style (67% compared with 100% of bottom-ranked ads). While top-ranked ads appeared more likely than others to use simulation/animation (25%), this difference was not statistically significant. 
 
 We compared the characteristics of the top-ranked 15% of ads in the overall sample with the characteristics of the middle-ranked 70% and bottom-ranked 15% of ads ( table 4 ). Regarding the key communication intent of the ad, the distribution of ads containing a ‘why change behaviour’ intent was significantly different across the three groups, with all of the top-ranked ads carrying a ‘why’ message but only half of the bottom-ranked ads doing so. In addition, 58% of the top-ranked ads featured information on the long-term harms of alcohol consumption, compared with 7% of middle-ranked ads and none of the bottom-ranked ads. (Not shown in table 4 , seven of the top-ranked ads featured information on long-term harms. Of these seven ads, six mentioned cancer, four mentioned stroke, two mentioned heart disease, two mentioned high blood pressure, one mentioned liver disease and one ad mentioned other non-specific ‘serious health problems’. In addition, of the four middle-ranked ads that featured long-term harms, cancer was mentioned in three and other non-specific ‘serious health problems’ were mentioned in one). A higher proportion of all top-ranked ads presented low-risk drinking guidelines (58%) compared with the middle-ranked (5%) and bottom-ranked ads (0%). 
 
 We assessed the degree of consistency in ad rankings across subgroups in two ways. First, we examined which ads were in the top-ranked 15% within each subgroup and the extent to which these overlapped with the top-ranked 15% for the overall sample ( table 3 ). Of the 12 ads that were top ranked in the overall sample, six were also top ranked among younger adults, nine were top ranked by older adults, seven were top ranked by men, eight were top ranked by women, ten were top ranked by low-risk drinkers and eight were top ranked by high-risk drinkers. More specifically, the ad ranked highest overall—Spread—was also ranked in the number one or two positions within each audience subgroup. Similarly, the second highest ranked ad overall—What you can't see—was ranked in second, third or fourth place in all subgroups except the low-risk drinkers (for whom it ranked 10th). The third highest ranked ad overall—Danny—was ranked in the top two or three in all subgroups except men (among whom it ranked 9th). We also examined the Spearman rank order correlation between the rankings of all 83 ads across the age, sex and risky drinking subgroups. The rank order of the 83 ads between the younger and older adults was significantly correlated, r s (81)=0.42, p<0.001. Similarly, the rank order of the 83 ads between men and women was significantly correlated, r s (81)=0.45, p<0.001, and so was the rank order of the 83 ads between low-risk and high-risk drinkers, r s (81)=0.46, p<0.001. 
 
 With a mean score of 3.77, the highest ranked ad was Spread, developed and funded by the Western Australian state government as part of their Alcohol and cancer mass media campaign. Ads ranked in the second to seventh positions—What you can't see (M=3.62) from the same Western Australian campaign, Danny (M=3.57) from New Zealand's Not the drinking campaign, Male (M=3.51) from the UK's Damage you can't see campaign, Could happen to you (M=3.45) also from the Western Australian Alcohol and cancer campaign, Female (M=3.44) from the Damage you can't see campaign and Change4Life (M=3.44) from the UK—all performed comparably with Spread in that they did not score significantly differently on the motivation outcome. From the eighth-ranked ad onwards, adjusted mean scores were significantly lower than for Spread. With a mean score of 2.42, the lowest ranked ad was Add nothing from the Not beersies campaign from New Zealand. Ads ranked in positions 81 and 82—Nails (M=2.64) and Piercings (M=2.69), both from Singapore's When to stop campaign—did not perform significantly better than Add nothing, whereas ads in position 80 and higher all scored significantly better than Add nothing ( table 2 ). 
 
 Around half of participants (46%) were classified as high risk for short-term alcohol-related harm and 31% were classified as high risk for long-term harm. When combined into the four-category variable, 51% were classified as low risk for short-term and long-term harm, 18% were at high risk of short-term harm but low risk of long-term harm, 3% were at low risk of short-term harm but high risk of long-term harm and 28% were at high risk of short-term and long-term harm ( table 1 ). When further aggregated for comparative analysis, overall 49% were high-risk drinkers (at risk of short-term and/or long-term harm) and the remaining 51% were low-risk drinkers. Risk proportions were similar to those calculated for adult weekly drinkers sourced from the 2013 National Drug Strategy Household Survey (NDSHS). 10 The proportion of 18–29 year olds in the sample (54%) was higher than in the NDSHS due to the use of age quotas during study recruitment. However, the sample was largely comparable with the NDSHS sample in terms of sex, residential location, SES, tertiary education and parental status ( table 1 ). 
 
 Discussion 
 
 The first aim of the study was to rank a large pool of alcohol harm reduction ads according to the extent to which adult weekly drinkers felt motivated by them to reduce their own alcohol consumption. Although motivation responses for all ads were within the middle range of the five-point scale (2.42–3.77), we identified several specific ads that topped the list and also identified the top-ranked 15% of ads and the message characteristics that significantly distinguished these from lower ranked ads. Campaign messages that drinkers found most motivating were those that directly communicated why change was advisable or necessary, rather than how to achieve such change, a finding consistent with that from tobacco control14 ,30 and obesity prevention.53 Top-ranked ads were also more likely to address long-term harms, conditions that are likely to reflect where most alcohol educational deficits exist.54 Emotional tone of the ads also differed across the three ranked categories, with ads featuring a positive tone more likely to be in the bottom-ranked 15% and top-ranked ads tending to be more likely to have a negative emotional tone (albeit not reaching statistical significance). This pattern of findings is broadly consistent with a recent small study of drinkers in the UK which found negative emotion mediated the effects of alcohol harm reduction ads on lower urges to drink.34 Inclusion of low-risk guidelines or recommendations was also more likely in top-ranked ads, suggesting this message element may have potency. Furthermore, although rankings varied somewhat, there was substantial overlap in the top-ranked ads across key demographic groups of younger and older adults, men and women and high-risk and low-risk drinkers, as was also reflected in the high correlations in rankings between subgroups. In particular, it was of interest to note how well the long-term harm ads performed with younger people, who might have been expected to self-exempt from these more distal harms. 
 
 To the best of our knowledge, this is the first published study to identify and comparatively evaluate a large pool of alcohol harm reduction ads from many different countries using a standard criterion outcome measure with a large sample of drinkers. As ads were only rated by Australian drinkers, it could be assumed that ads produced in Australia would have been rated more highly than others. However, we found that the top-ranked 15% of ads was comprised of ads from Australia (six ads), the UK (four ads) and New Zealand (two ads), and we also found no significant differences in the distribution of ads across ranking categories by country of origin. By controlling for familiarity with the ads in our analyses, we further minimised the potential effect of country of production on responses to the ads. A study strength was that all ads were presented in a standard way, achieving consistent exposure. On the other hand, forced exposure may not reflect how viewers might respond in a natural media viewing situation where exposure occurs repeatedly over a longer duration. Another issue is that online non-probability panels do not provide a random population sample, and so we do not suggest our parameter estimates represent the national population statistically. However, online panels are typically used in the advertising industry to predict consumer responses to advertising, and the patterns of ad-elicited motivation observed in this large and varied sample are likely to reflect those in the population, particularly given the similarities between our sample's demographic and alcohol consumption characteristics with those of the benchmark national survey. 
 
 Another limitation was that our outcome measure was felt motivation to reduce drinking rather than drinking behaviour change. In their description of the ‘Big Five Principles of Behaviour Change’, Hill and Dixon (2010) describe motivation as being a necessary condition for volitional behaviour, but they note that it is often insufficient on its own.55 Mass media campaigns (and other behaviour change programmes) can also address the other key principles of behaviour change, by modelling the desired behaviour (as demonstrated in the how-to-change behaviour ads in our sample), building capacity for change (by advocating for policy change), enabling people to remember the recommended behaviours (by ensuring sufficient campaign exposure and repetition at regular intervals) and providing reinforcement for the desired behaviour (by demonstrating the negative consequences of failing to reduce alcohol consumption).55 Further research could investigate the extent to which the effectiveness of alcohol harm reduction ads may be enhanced by addressing these other determinants of behaviour change. 
 
 Collectively, this information may guide countries to develop campaign messages with the key features identified here, or to select any of the existing top-ranked ads with most potential to motivate change in adult drinking behaviour for broadcast in their own jurisdictions. Given the substantial upfront costs and resources involved in developing mass media campaigns, recycling existing campaign materials can help to ensure that scarce campaign resources can be directed towards achieving sufficient population exposure.56 ,57 It is notable that the two highest ranked ads in this study—Spread and What you can't see—predominantly consisted of animated imagery of the internal harms caused by alcohol (which are applicable to all people), rather than footage of models or settings that could be more culturally specific. These two ads are particularly suitable for low-cost adaptation for use in countries other than Australia given that the major adaptation required would be to revoice the ads and translate the final tagline. Recent tobacco control research has demonstrated the viability of adapting campaign messages shown to be effective in one setting for use in other jurisdictions.57 Studies comparing responses from smokers in 10 different countries found high levels of consistency in responses to different tobacco control ads across countries and demographic subgroups, particularly when these ads used graphic images to depict the physical effects of smoking in a direct and evocative manner.28 ,29 We therefore recommend that the current findings be used by jurisdictions to identify those ads that, following local pretesting and any necessary adaptations for language and taglines, may help to motivate reduced alcohol consumption within their own adult populations. 
 
 In addition, our finding of consistent ad rankings across audience subgroups suggests that a ‘common denominator approach’ could have merit, thereby making scant resources go further.36 That is, by carefully selecting ads that appeared in the top-ranked category for all or most of the audience subgroups, countries could use a single campaign approach to motivate key demographic groups to reduce their drinking, while also resonating with the wider population to stimulate a broader cultural change process. However, we note that it is possible that the age groups compared in this study (18–29 year olds vs 30–64 year olds) were too broad to adequately capture variation in the range of responses to alcohol harm reduction ads across the age spectrum. Although all of our predicted mean scores on the motivation outcome were adjusted for age (including in the age-stratified models), future research may benefit from a more fine-grained segmentation when considering the effects of age in determining responses to alcohol harm reduction campaigns. 
 
 The promising performance of ads that carried a guideline message suggests that more widespread and systematic promotion of drinking guidelines accompanied by good reasons to limit consumption could serve to provide a new anchoring point for decisions about consumption58 and shift public attitudes about alcohol.59 While there has been debate as to whether disseminating guidelines could confuse or backfire60 or even be relevant when many drinkers rely so much on their own sensed experience of how much they can drink,61 some suggest that there is a moral imperative to inform consumers62 and recent empirical observations provide reasons for optimism regarding their potential effectiveness.59 ,63 
 
 This study has identified specific campaign messages that offer the most potential to increase motivation to reduce alcohol consumption in the broader population, as well as in key demographic and high-risk drinker subgroups. This information makes an important contribution to the limited evidence base on the potential for mass media campaigns to reduce alcohol-related harm. Although we noted earlier that perceived effectiveness measures—of which the motivation outcome used here is one—predict behaviour change for tobacco control ads,41 ,42 further studies should examine the predictive validity of this and other perceived effectiveness outcomes for subsequent reduced drinking behaviour. Further research is also necessary to validate our assumption that the ads that performed most strongly among Australian drinkers would similarly impact drinkers in other jurisdictions. It would also be of interest to examine if certain long-term harms are more motivating than others, given six out of seven of the long-term harm ads in the top-ranked 15% of ads specifically mentioned cancer. Overall, our findings suggest there may be promise in resourcing alcohol harm reduction campaigns that educate audiences about why they may need to change their drinking by providing information about the long-term harms of risky alcohol use and communicating guidelines for low-risk drinking.
– If you want to get people to stop boozing it up, don't show them images of glasses of healthy, sparkling water instead of beer—show them an ad that illustrates how too many cocktails can cause cancer to course through their bodies, the Guardian reports. That's the finding of a new study published in the BMJ Open journal that examined English-language alcohol ads to identify which ones proved best at inspiring drinkers to cut down. Researchers tapped a pool of 2,174 Australian adults ages 18 to 64 who drink alcohol at least one or two days a week. A total of 83 ads were shown, and the subjects were instructed to note after viewing each one how motivated they were to reduce their drinking on a scale from one to five, with "one" counting as an unmotivated "Nah, I'm good," and "five" as "Take the key to my liquor cabinet and bury it, please." The most effective ad: "Spread," a 30-second video created by the Western Australian government a few years ago that shows the cancerous mutations wrought after alcohol gets into one's bloodstream. The dud: that ad pushing water over beer. Cancer Council Victoria CEO Todd Harper tells the Guardian that "Spread" may have made an impact because folks simply don't know alcohol is a Group 1 carcinogen, the most dangerous category. Even though Fergus Taylor, the director of Alcohol Beverages Australia, calls the "Spread" ad "scaremongering," Harper notes "every drink" ups one's chance of getting cancer, including that of the mouth, liver, and bowel. What these findings should do is spur campaigns that maximize the public's awareness of alcohol so they can cut their cancer risk, Harper says, per Mumbrella. (A study says alcohol can be directly tied to seven cancers.)