Cancer, Reproductive, Cardiovascular, and Other Chronic Disease Prevention Program

Burden

Many sources of data exist on occupational carcinogens, including data concerning single agents and complex mixtures as preventable causes of occupational cancer and occupational groups at high risk for cancer.⁵ Epidemiologic studies, within specific industries and/or addressing specific exposures, have identified elevated cancer risks among workers. These studies are too numerous to detail here. Among recent examples, a published update of the mortality status of 7,800 workers exposed to solvents in the manufacture of shoes revealed an excess of lung cancer deaths (standardized mortality ration=1.36, 95% confidence interval=1.19-1.54).⁶ This study supports a possible association between lung cancer mortality and exposure to chronic, low levels of organic solvents, a finding supported by other studies.

Surveillance systems are available that provide data addressing potentially occupationally-related cancer. The NIOSH National Occupational Mortality Surveillance System is a database of death certificate data with coded occupation and industry information. Investigators can use these data to survey association of cause-specific mortality and occupation and/or industry. The measure of association used most often in this system is the proportionate mortality ratio. For example, this database can be used to survey associations of cancer (or other health outcomes such as heart disease) mortality among persons from different occupations. Regarding lung cancer specifically, surveillance information is available from sources including the Work-Related Lung Disease Surveillance System. This surveillance activity provides data, presented in table, chart, and map format, for a variety of work-related respiratory conditions including lung cancer.

Need

There are many known or potential carcinogens that are understudied. One of the goals of CRC research is to follow-up on cohorts of previous studies to continue to increase our knowledge about exposures, interventions, and health effects. Information on exposure and cancer risk derived from studies of high-priority agents should be used to develop quantitative risk assessment models, upon which authoritative recommendations may be based.

Impact

NIOSH research has identified physical and chemical agents in the workplace associated with cancer, including asbestos, benzene, benzidene, 1,3-butadiene, cadmium, chromium, crystalline silica, dioxin, formaldehyde, vinyl chloride, and others. NIOSH studies continue to find links between cancer and workplace exposure to certain chemicals, including most recently beryllium, diesel exhaust, o-toluidine, and 1-bromopropane. A recent NIOSH study showed that a population of 30,000 firefighters from three large cities had higher rates of several types of cancers, and of all cancers combined, than the U.S. population as a whole. NIOSH research informs recent guidance to prevent work-related cancer by the World Health Organization and the National Toxicology Program, which cite NIOSH publications documenting the cancer-causing potential of work-related chemical exposures.

⁵ Overview of preventable industrial causes of occupational cancer. Environ Health Perspect 1995; 103:197-203.

⁶ Mortality of workers employed in shoe manufacturing: An update. AJIM 2006; 49:535-546.

Burden

Heart disease is the major single cause of mortality in the United States, accounting for 23.4% of deaths in 2014.⁷ Little is known about occupational risks for heart disease. A few specific toxins encountered occupationally are known to affect the heart, including carbon disulfide, nitroglycerin, carbon monoxide and environmental tobacco smoke. For example, concerning environmental tobacco smoke, a large prospective epidemiologic study by NIOSH CRC investigators and others found approximately 20% higher coronary heart disease death rates among never smokers exposed to environmental tobacco smoke.⁸ A risk assessment addressing occupational settings has determined that exposure to environmental tobacco smoke is associated with increased risk of death from ischemic heart disease among nonsmoking U.S. workers.⁹

Need

There is a need for increased epidemiologic research into occupational factors contributing to cardiovascular disease among workers.¹⁰ Opportunities exist to utilize existing study populations and possibly stored biological specimens to pursue new research questions that would enhance our knowledge concerning the role of occupational exposures in cardiovascular disease. In addition, recently emerging exposures (e.g. nanotechnology) may require assessment in newly established cohorts and new laboratory-based studies through collaborative research efforts involving NIOSH and its partners. Development of new methods that enable improved detection of exposure and identification of sub-clinical cardiovascular disease should make important contributions.

Impact

The path between the conduct of research and its eventual resulting changes in practice can be long and indirect for epidemiologic and laboratory-based studies, but research leading to a better understanding of the biologic mechanisms underlying cardiovascular disease is vital to achieving reductions in workplace-attributable cardiovascular disease.

⁷ Heron M. Deaths: Leading Causes for 2014. National vital statistics reports; vol 65 no 5. Hyattsville, MD: National Center for Health Statistics. 2016.  https://www.cdc.gov/nchs/data/nvsr/nvsr65/nvsr65_05.pdf .

⁸ Environmental tobacco smoke and coronary heart disease in the ACS CPS-II cohort. Circulation 1996. 94:622-628.

⁹ Risk assessment for heart disease and workplace ETS exposure among nonsmokers. Env Health Persp 1999; 107(S6):859-863.

¹⁰ Epidemiology of occupation and coronary heart disease: research agenda. AJIM 1996; 30:495-499.

Burden

There is significant public health concern about potential effects of occupational exposures on reproductive outcomes. Examples of substances with reported reproductive or developmental effects still in regular commercial use include heavy metals (such as lead), solvents, and pesticides. A recent example includes an evaluation of workplace exposure from a microelectronics and business machines manufacturing facility which suggests an association between paternal exposure to metals (primarily lead) and increased ventricular septal defect risk in infants.¹¹ Estimates of adverse reproductive outcomes demonstrate widespread impact—for example, it is estimated that 10% to 20% of recognized pregnancies end in spontaneous abortion, and that 3% of all live births have major malformations.¹² Others have estimated that 3% of major malformations are due to toxicant exposure, 23% are due to multifactorial causes, and 40% are due to unknown causes.^13-15 Despite the public health concern and the widespread impact, progress has been limited in identifying occupational reproductive hazards and in separating the contributions of potential occupational hazards from other etiologic factors.

Need

There is significant public health concern about the potential effects of occupational exposure to toxic substances on reproductive outcomes. Several toxicants with reported reproductive and developmental effects are still in regular commercial or therapeutic use and thus present potential exposure to workers. Examples of these include heavy metals, organic solvents, pesticides and herbicides, and sterilants, anesthetic gases, and anticancer drugs used in health care. Many other substances are suspected of producing reproductive or developmental toxicity but lack sufficient data. Progress has been limited in identifying hazards and quantifying their potencies and in separating the contribution of these hazards from other etiologic factors. The pace of laboratory studies to identify hazards and to underpin the biologic plausibility of effects in humans has not matched the pace at which new chemicals are introduced into commerce. Though many research challenges exist today, recent technologic and methodologic advances have been made that allow researchers to overcome some of these obstacles. One of the goals of the NIOSH CRC program, in collaboration with many partners, is to take advantage of recent technologic and methodologic advances in reproductive health research to improve health and reduce adverse reproductive health outcomes.

Impact

Identifying the causative agents, mechanisms by which they act, and any potential target populations will present the opportunity to intervene and better protect the reproductive health of workers.

¹¹ Silver SR [2016]. Birth defects in infants born to employees of a microelectronics and business machine

manufacturing facility. Birth Defects Research (Part A). [published online ahead of print 25 May 2016]. doi:10.1002/bdra.23520.

¹² An occupational reproductive research agenda for the third millennium. Env Health Perspectives 2003; ¹¹1(4):584-592.

13 Impact of the detection and prevention of developmental abnormalities in human studies. Reprod Toxicol 1997; 11:267-269.

¹⁴ Introduction to the symposium. Reprod Toxicol 1997; 11:261-263.

¹⁵ Frequency of human congenital malformations. Clin Perinatol 1986; 13(3):545-554.

Other examples of peer-reviewed literature that may be sources of information on which to guide future work of the CRC include the following:

Prioritization of NTP reproductive toxicants for field studies
Reprod Toxicol 2000; 14(4):293-301.
This article describes a systematic method for prioritizing chemicals that may need human reproductive health field studies.

Priorities for development of research methods in occupational cancer
Env Health Perspectives 2003; 111(1):1-12.
This article identifies needs and gaps in occupational cancer research methods in four broad areas: identification of occupational carcinogens, design of epidemiologic studies, risk assessment, and primary and secondary intervention.