PAH exposure and oxidative stress indicators of human cohorts exposed to traffic pollution in Lahore city (Pakistan)

Epigenetic markers of exposure to polycyclic aromatic hydrocarbons in Mexican brickmakers: A pilot study

PAH exposure biomarkers are associated with clinico-chemical changes in the brick kiln workers in Pakistan.

Objectives Diesel engine exhaust (DEE) is a ubiquitous environmental pollutant and is carcinogenic to humans. To seek early and sensitive biomarkers for prediction of adverse health effects, we analysed the components of DEE particles, and examined the genetic and oxidative damages in DEE-exposed workers. Methods 101 male diesel engine testing workers who were constantly exposed to DEE and 106 matched controls were enrolled in the present study. The components of DEE were analysed, including fine particulate matter (PM 2.5 ), element carbon (EC), nitrogen dioxide (NO 2 ), sulfur dioxide (SO 2 ) and polycyclic aromatic hydrocarbons (PAHs). Postshift urine samples were collected and analysed for 1-hydroxypyrene (1-OHP), an internal exposure marker for DEE. Levels of DNA strand breaks and oxidised purines, defined as formamidopyrimidine-DNA glycosylase (FPG) sites in leucocytes, were measured by medium throughput Comet assay. Urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) was also used to determine the level of oxidative stress. Results We found higher levels of PM 2.5 , EC, NO 2 , SO 2 and PAHs in the diesel engine testing workshop and significantly higher urinary 1-OHP concentrations in exposed subjects (p Conclusions These findings suggest that DEE exposure mainly induces DNA damage, which might be used as an early biomarker for risk assessment of DEE exposure.

https://oem.bmj.com/content/oemed/73/2/83.full.pdf

Long-term exposure to diesel engine exhaust induces primary DNA damage: a population-based study

Virtually all human disease is induced by oxidative stress. Oxidative stress, which is caused by toxic environmental exposure, the presence of disease, lifestyle choices, stress, chronic inflammation or combinations of these, is responsible for most disease. Oxidative stress from all sources is additive and it is the total oxidative stress from all sources that induces the onset of most disease. Oxidative stress leads to lipid peroxidation, which in turn produces Malondialdehyde. Serum malondialdehyde level is an additive parameter resulting from all sources of oxidative stress and, therefore, is a reliable indicator of total oxidative stress which can be used to predict the onset of disease in clinically asymptomatic individuals and to suggest the need for treatment that can prevent much human disease.

/pdf/review-article-predicting-disease-onset-in-clinically-23514jbj03.pdf

Review article. Predicting disease onset in clinically healthy people

Objectives: To investigate associations between occupational exposure to cooking oil fumes (COFs) and potential oxidative and genotoxic effects in kitchen workers. Methods: Sixty-seven male kitchen workers and 43 male controls from Chinese restaurants in Guangzhou were recruited. For all the participants, the levels of 1-hydroxypyrene (1-OHP) and 8-hydroxy-2-deoxyguanosine (8-oxodG) in urine, binucleated micronucleus (BNMN) frequency, comet tail length and tail DNA% in peripheral blood lymphocytes (PBLs) and malondialdehyde (MDA) and superoxide dismutase (SOD) in serum were measured. The inhalable particulates (PM10) in their workplaces were also monitored. Results: Our results showed that the exposed group had a significantly higher median level of urinary 1-OHP than that of the control group (p<0.01). In addition, the median levels of 8-oxodG, BNMNs, tail length and MDA in the exposed group were markedly higher than those of the controls (p<0.01). These differences, except that of MDA, appeared not to be modified by the potential confounders: age, BMI, smoking and alcohol consumption. A univariate regression analysis showed that greater 1-OHP, 8-oxodG, BNMNs, tail length and MDA were associated with years working in a kitchen and cooking time per day. All these positive associations remained after adjusting for the four confounders in a subsequent multivariate linear regression analysis. Conclusions: Occupational exposure to COFs led to increased oxidative damage in Chinese kitchen workers. The health consequences of these oxidative changes need further investgation. Urinary 1-OHP and 8-oxodG are noninvasive and effective biomarkers for assessment of oxidative damage in restaurants workers.

/pdf/elevated-oxidative-damage-in-kitchen-workers-in-chinese-319rz7ciq2.pdf

Bin Xu

Papers

Elevated Oxidative Damage in Kitchen Workers in Chinese Restaurants