Little is known about the possible association between occupational exposure to mineral particulate matters and change in leukocyte telomere length (LTL) as a hallmark of aging. The present study studied the relationship between occupational exposures to mineral dust and LTL in the exposed group of workers and compared to non-exposed workers. One hundred and ten male workers (80 exposed and 30 non-exposed) from different units of a ceramic factory were recruited in the study. Personal air samples were collected in the breathing zone of the workers for inhalable and respirable fractions. Relative LTL was measured in blood genomic DNA using the quantitative real-time PCR method and expressed as telomere/single copy gene ratio. Exposure to inhalable and respirable dusts in the exposed group was 22.66 ± 52.38 and 2.54 ± 9.34 mg/m respectively. Inhalable and respirable exposure values were highly correlated (r = 0.43; p < 0.001). Exposure to respirable and inhalable particles in 38.75% and 8.75% of exposed workers was higher than threshold limit value respectively. Mean LTL in the exposed workers (0.64 ± 0.06) was significantly shorter than the non-exposed workers (0.73 ± 0.07) (p < 0.001). Despite the significant difference in exposure intensity according to working units in the exposed group, there was no significant difference in LTL according to the working units (p = 0.60). In the adjusted regression models, but not crude models, marginally significant and positive association was found between both size fractions and LTL. The observed effect size for respirable particles was five times of that found for the inhalable fraction (beta 0.005 and 0.001 respectively). Mineral dust-and not only traffic-related air pollutant exposure-could be regarded as a risk factor in the process of cell aging. Our findings imply that early biological aging, as reflected in telomere shortening, may mediate the effects of occupational air pollution exposure on human health.
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