NIOSH manual of analytical methods, fifth edition. Ashley K, O'Connor PF, eds. Cincinnati, OH: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, DHHS (NIOSH) Publication No. 2014-151, 2016 Apr; :DL1-DL41
Over a million U.S. workers (e.g., trucking, mining, railroad, construction, agriculture) are occupationally exposed to diesel exhaust [NIOSH 1988]. The widespread use of diesel-powered equipment is a recognized health concern. Exposure to diesel exhaust is associated with an increased risk of lung cancer [Attfield et al. 2012; Garshick et al. 2004; HEI 1995; IARC 2012; Silverman et al. 2012]. Diesel exhaust is pervasive, and environmental exposure is a public health concern; but workplace exposures pose higher risk because they are generally much higher than those encountered by the general population. In 1988, the National Institute for Occupational Safety and Health (NIOSH) reported diesel exhaust as a potential occupational carcinogen and recommended that employers reduce workers' exposures [NIOSH 1998]. This recommendation was based on five independent animal studies, in which rats exposed to unfiltered exhaust showed an increased incidence of benign and malignant lung tumors [IARC 1989]. Other organizations, including the International Agency for Research on Cancer (IARC) [IARC 1989], the World Health Organization (WHO) [WHO 1996], the California Environmental Protection Agency [CalEPA 1998], the U.S. Environmental Protection Agency (EPA) [EPA 2000a], and the National Toxicology Program [NTP 2000] reviewed the animal and human evidence, and each classified diesel exhaust as a probable human carcinogen or similar designation. In 2012, based on epidemiological studies, IARC [IARC, WHO 2012] reclassified diesel exhaust as carcinogenic to humans (Group 1). In particular, a major study of U.S. miners, conducted by NIOSH and the National Cancer Institute (NCI), found increased risk of death from lung cancer in exposed workers [Attfield et al. 2012; Silverman et al. 2012]. Noncancer health effects also are associated with diesel exhaust exposure, including immunologic, respiratory, and cardiovascular effects. Diesel exhaust particles can act as nonspecific airway irritants at relatively high exposures. At lower levels, they can trigger release of mediators (cytokines, chemokines, immunoglobulins, and oxidants) of allergic and inflammatory responses [Pandya et al. 2002]. Diesel particles may promote expression of the immunologic response phenotype (Th2) associated with asthma and allergic disease and may have greater immunologic effects in the presence of environmental allergens. Internationally, the prevalence of asthma (and related hospitalizations and mortality) continues to rise in adults and children. Children may be more vulnerable than adults [Edwards et al. 1994; Weiland et al. 1994; Wjst et al. 1993; van Vlient et al. 1997]. Studies indicate children living along major trucking thoroughfares are at increased risk for asthmatic and allergic symptoms. In the United States, the number of individuals with self-reported asthma increased by 75% from 1980 to 1994 [Mannino et al. 1998]. The immunologic evidence is consistent with results of epidemiologic studies that associate traffic-related air pollution, especially diesel exhaust particles, with an increase in respiratory diseases. Studies have consistently found positive associations between particulate air pollution and daily mortality [Brown et al. 2000; Dockery et al. 1993; EPA 1999, 2000b; Pope et al. 1995a; Pope et al. 1995b; Pope et al. 2002; Samet 2000; Schwartz 1997; Schwartz et al. 1996]. The traditional U.S. air quality standard for particulate matter is based on particles having diameters ≤ 10um (PM10) [52 Fed. Reg. 24634 (1987)]. In 1997, EPA proposed a new standard [62 Fed. Reg. 38652 (1997)] based on particles having diameters ≤ 2.5 um (PM2.5). These smaller particles originate mainly from combustion sources. The new standard was proposed because recent studies had found higher correlation between fine particle pollution and adverse health effects. In an analysis [Schwartz et al. 1996] of data from six U.S. cities, fine particles were consistently associated with increased risk of death from chronic obstructive pulmonary disease, pneumonia, and ischemic heart disease. Positive associations between fine particle pollution and hospital admissions due to respiratory and cardiovascular illness also have been found [Schwartz 1994; Burnett et al. 1995; Schwartz and Morris 1995]. Particles produced by combustion sources were implicated in these findings. In addition to asthma, chronic inhalation of diesel exhaust particles may play a role in these adverse health outcomes. Reviews on the health effects of diesel exhaust have been published [CalEPA 1998; EPA 2000a; HEI 1995, 2002; IARC 1989; IARC (WHO) 2012; NIOSH 1988; NTP 2000; Solomon et al. 1998; WHO 1996].
Diesel emissions; Diesel exhausts; Diesel exhaust; Workers; Work environment; Exposure levels; Risk factors; Trucking; Mining; Railroad industry; Construction; Construction industry; Agricultural industry; Agriculture; Health effects; Lung disorders; Cancer; Carcinogens; Animals; Laboratory animals; Immunologic disorders; Respiratory system disorders; Cardiovascular system disorders; Particulates