There are concerns about the health effects of formaldehyde exposure, including carcinogenicity, in light of elevated indoor air levels in new homes and occupational exposures experienced by workers in health care, embalming, manufacturing, and other industries. Epidemiologic studies suggest that formaldehyde exposure is associated with an increased risk of leukemia. However, the biological plausibility of these findings has been questioned because limited information is available on the ability of formaldehyde to disrupt hematopoietic function. Our objective was to determine if formaldehyde exposure disrupts hematopoietic function and produces leukemia-related chromosome changes in exposed humans. We examined the ability of formaldehyde to disrupt hematopoiesis in a study of 94 workers in China (43 exposed to formaldehyde and 51 frequency-matched controls) by measuring complete blood counts and peripheral stem/progenitor cell colony formation. Further, myeloid progenitor cells, the target for leukemogenesis, were cultured from the workers to quantify the level of leukemia-specific chromosome changes, including monosomy 7 and trisomy 8, in metaphase spreads of these cells. Among exposed workers, peripheral blood cell counts were significantly lowered in a manner consistent with toxic effects on the bone marrow and leukemia-specific chromosome changes were significantly elevated in myeloid blood progenitor cells. These findings suggest that formaldehyde exposure can have an adverse effect on the hematopoietic system and that leukemia induction by formaldehyde is biologically plausible, which heightens concerns about its leukemogenic potential from occupational and environmental exposures.

The combustion of biomass and coal is the dominant source of household air pollution (HAP) in China, and contributes significantly to the total burden of disease in the Chinese population. To characterize HAP exposure related to solid fuel use and ventilation patterns, an exposure assessment study of 163 nonsmoking female heads of households enrolled from 30 villages was conducted in Xuanwei and Fuyuan, two neighboring rural counties with high incidence of lung cancer due to the burning of smoky coal (a bituminous coal, which in health evaluations is usually compared to smokeless coal—an anthracite coal available in some parts of the area). Personal and indoor 24-h PM2.5 samples were collected over two consecutive days in each household, with approximately one-third of measurements retaken in a second season. The overall geometric means (GM) of personal PM2.5 concentrations in Xuanwei and Fuyuan were 166 [Geometric Standard Deviation (GSD):2.0] and 146 (GSD:1.9) μg/m3, respectively, which were similar to the indoor PM2.5 air concentrations [GM(GSD):162 (2.1) and 136 (2.0) μg/m3, respectively]. Personal PM2.5 was moderately highly correlated with indoor PM2.5 (Spearman r = 0.70, p < 0.0001). Burning wood or plant materials (tobacco stems, corncobs etc.) resulted in the highest personal PM2.5 concentrations (GM:289 and 225 μg/m3, respectively), followed by smoky coal, and smokeless coal (GM:148 and 115 μg/m3, respectively). PM2.5 levels of vented stoves were 34–80% lower than unvented stoves and firepits across fuel types. Mixed effect models indicated that fuel type, ventilation, number of windows, season, and burning time per stove were the main factors related to personal PM2.5 exposure. Lower PM2.5 among vented stoves compared with unvented stoves and firepits is of interest as it parallels the observation of reduced risks of malignant and nonmalignant lung diseases in the region.