Search

This paper reports findings from a screening study conducted to examine potential lead (Pb) exposures in residents of a Mexican village where Pb oxide continues to be used in ceramic pottery production. Extremely high Pb concentrations were measured in personal and indoor air samples, household surface dust samples, and household soil samples. Personal air Pb concentrations for workers performing pottery firing and glazing were up to 454 μg/m[SUP3]. Results from indoor air samples indicate that airborne Pb concentrations were lower during nonglazing period compared to the glazing period. Soil Pb concentrations measured in 17 homes ranged from 0.39 to 19,8 mg/g. Dust Pb loading on surfaces of household items, hands, and clothes of a worker ranged from 172 to 33 060 μg/ft[SUP2]. Pb content as high as 2.4 μg/g was found in a bean stew cooked in a pot made in the village. Based on these Pb concentrations measured in multiple media and data adapted for exposure contact rates, we have made rough estimates of Pb exposures via inhalation, soil/dust ingestion, and food ingestion. Estimated total daily Pb intake, on average, is 4.0 mg for adults and 3.4 mg for children living in the village. In the total daily intake, a greatest fraction may be contributed by food ingestion and another significant fraction may come from soil/dust ingestion for the children. Although the sample size is small, these measurements indicate a very significant public health problem for the village residents and a large number of other similar communities in Mexico. (It was estimated that there are approximately 1.5 million glaze potters.) The Pb exposure is implicated in a number of pervasive health problems in the region, and is the cause for national and international attention. Several recommended solutions to this problem range from personal protection and behavioral changes to introduction of altemative glazes. [ABSTRACT FROM AUTHOR]

Exposure to air pollution particulate matter (PM) and tuberculosis (TB) are two of the leading global public health challenges affecting low and middle income countries. An estimated 4.26 million premature deaths are attributable to household air pollution and an additional 4.1 million to outdoor air pollution annually. Mycobacterium tuberculosis (M.tb) infects a large proportion of the world's population with the risk for TB development increasing during immunosuppressing conditions. There is strong evidence that such immunosuppressive conditions develop during household air pollution exposure, which increases rates of TB development. Exposure to urban air pollution has been shown to alter the outcome of TB therapy. Here we examined whether in vitro exposure to urban air pollution PM alters human immune responses to M.tb. PM2.5 and PM10 (aerodynamic diameters <2.5μm, <10μm) were collected monthly from rainy, cold-dry and warm-dry seasons in Iztapalapa, a highly populated TB-endemic municipality of Mexico City with elevated outdoor air pollution levels. We evaluated the effects of seasonality and size of PM on cytotoxicity and antimycobacterial host immunity in human peripheral blood mononuclear cells (PBMC) from interferon gamma (IFN-γ) release assay (IGRA)+ and IGRA- healthy study subjects. PM10 from cold-dry and warm-dry seasons induced the highest cytotoxicity in PBMC. With the exception of PM2.5 from the cold-dry season, pre-exposure to all seasonal PM reduced M.tb phagocytosis by PBMC. Furthermore, M.tb-induced IFN-γ production was suppressed in PM2.5 and PM10-pre-exposed PBMC from IGRA+ subjects. This observation coincides with the reduced expression of M.tb-induced T-bet, a transcription factor regulating IFN-γ expression in T cells. Pre-exposure to PM10 compared to PM2.5 led to greater loss of M.tb growth control. Exposure to PM2.5 and PM10 collected in different seasons differentially impairs M.tb-induced human host immunity, suggesting biological mechanisms underlying altered M.tb infection and TB treatment outcomes during air pollution exposures., Competing Interests: The authors have declared that no competing interests exist.

Rationale: Associations between urban (outdoor) airborne particulate matter (PM) exposure and TB and potential biological mechanisms are poorly explored., Objectives: To examine whether in vivo exposure to urban outdoor PM in Mexico City and in vitro exposure to urban outdoor PM 2.5 (< 2.5 µm median aerodynamic diameter) alters human host immune cell responses to Mycobacterium tuberculosis ., Methods: Cellular toxicity (flow cytometry, proliferation assay (MTS assay)), M. tuberculosis and PM 2.5 phagocytosis (microscopy), cytokine-producing cells (Enzyme-linked immune absorbent spot (ELISPOT)), and signalling pathway markers (western blot) were examined in bronchoalveolar cells (BAC) and peripheral blood mononuclear cells (PBMC) from healthy, non-smoking, residents of Mexico City (n=35; 13 female, 22 male). In vivo-acquired PM burden in alveolar macrophages (AM) was measured by digital image analysis., Measurements and Main Results: In vitro exposure of AM to PM 2.5 did not affect M. tuberculosis phagocytosis. High in vivo-acquired AM PM burden reduced constitutive, M. tuberculosis and PM-induced interleukin-1β production in freshly isolated BAC but not in autologous PBMC while it reduced constitutive production of tumour necrosis factor-alpha in both BAC and PBMC. Further, PM burden was positively correlated with constitutive, PM, M. tuberculosis and purified protein derivative (PPD)-induced interferon gamma (IFN-γ) in BAC, and negatively correlated with PPD-induced IFN-γ in PBMC., Conclusions: Inhalation exposure to urban air pollution PM impairs important components of the protective human lung and systemic immune response against M. tuberculosis . PM load in AM is correlated with altered M. tuberculosis -induced cytokine production in the lung and systemic compartments. Chronic PM exposure with high constitutive expression of proinflammatory cytokines results in relative cellular unresponsiveness., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.)