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Cardiovascular disease (CVD) kills and disables millions of people worldwide. Indeed, analysis of disability-adjusted life years shows that CVD is the major contributor to loss of health to mortality and disability in several continents.1 One major contributor to CVD is work environment which can involve multiple risk factors, including exposure to smoke, chemicals and other potentially harmful environmental conditions. Despite substantial research into CVD risk factors and other occupational diseases such as cancer, occupational CVD has not yet been well investigated. For example, we have limited knowledge about the risk factors for occupational CVD, and in particular, if some groups have increased susceptibility, including genetic, to specific risk factors.
Some non-chemical risk factors for occupational CVD have been identified, such as noise exposure at work, shift work, physical (in)activity at work and mentally stressful work with a lack of control.2 Less is known about chemical risk factors, but associations have been established between CVD and certain toxicants (eg, silica dust, welding fumes and engine exhaust). Associations also exist for exposure to arsenic, benzopyrenes, lead, dynamite, carbon disulphide, carbon monoxide, particulate matter, metalworking fluids and occupational exposure to tobacco smoke.3–5 However, while individual studies have indicated that physical and chemical factors might increase the risk of CVD,2 3 recent reviews have concluded that not enough high-quality studies have been made to be able to establish an association.3
To help remedy this lack of information, in a study published in Heart, Bulka et al 6 examine the link between CVD and chemical exposure. The authors focus on Hispanic and Latino workers, a large minority population in the USA, and estimate the proportion of workers exposed to solvents, metals or pesticides in the workplace. Their findings suggest that less than 10% of employed Hispanics/Latinos were exposed to any of these compounds. Furthermore, they report that in this group of workers, occupational exposures to metals or pesticides, in particular, were associated with an elevated prevalence of coronary heart disease and atrial fibrillation. The strengths of the study are that they use a community-based cohort design which may mitigate the bias of healthy worker selection; there is information about several lifestyle and intermediate outcomes, for example, hypertension, and BMI; and that they focus on a vulnerable working group. Hispanic/Latinos were hypothesised to be more exposed to cardiotoxic agents from taking hazardous jobs with low levels of protection, due to low socioeconomic status and language barriers.
The study found the strongest associations for metals and pesticides and coronary heart disease and atrial fibrillation, and further work should focus on which biological mechanisms play a role for metal-associated and pesticide-associated CVD. Many metals are strong inducers of oxidative stress which may result in CVD either directly or via increased inflammation. Association between pesticides and CVD are less well studied, and although some pesticides cause oxidative stress, other mechanisms are likely to be important. Further, it is necessary to identify which metals and pesticides may be the most influential and if there are synergistic effects. The present study evaluated one exposure at a time without adjustments for other occupational risk factors for CVD. Moreover, no analysis was performed to evaluate the combined effect of these exposures in association with CVD (probably due to low power), even though many workers are exposed to a mixture of occupational CVD risk factors. Obviously, more studies of this topic is needed in the future.
Exposure to metals and pesticides is common worldwide, and this study highlights the need to better understand the risks that these exposures cause, and to limit exposure in the workplace, thus promoting cardiac health.
Footnotes
Contributors KB has written this editorial.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent Not required.
Provenance and peer review Commissioned; internally peer reviewed.
Linked Articles
- Cardiac risk factors and prevention