Relationship Between Air Pollution and Lung Cancer in Fujian Province: A Case-Control Study

Background:Outdoor air pollutants, especially particulate matters, are defined as a type of carcinogen by the International Agency for Research on Cancer. Studies have shown that air pollutionis associated with lung cancer morbidity or mortality. This study is aimed at exploring the relationship between air pollutants and primary lung cancer in Fujian Province, China. Methods:We conducted a hospital-based, retrospective, case–control epidemiological study on three different populations to assess the occurrence of lung cancer caused by exposure to various levels of air pollution. Statistical analysiswas performed using the SPSS 25.0. Unconditional logistic regression modeling and identification of possible confounding factors were performed by calculating odds ratios (ORs) and 95% confidence intervals (CIs) for air pollution indexes and lung cancer risk. Results: The total study population comprised 885 lung cancer patients and 1,220 healthy controls. The following parameters were identified as risk factors for lung cancer among the total population: smoking; exposure to cooking oil fumes; passive smoking; medical history of lung disease; family history of lung cancer; and exposure to PM10, PM2.5, and O3. Fruit intake and physical exercise were protective against lung cancer. For smokers, medical history of lung disease, family history of lung cancer, and exposure to PM10, and PM2.5 were risk factors for lung cancer, while fruit intake and physical exercise were protective factors. Among non-smokers, exposure to cooking oil fumes; medical history of lung disease; family history of lung cancer; and exposure to PM10, PM2.5, and O3 were factors increasing the risk of lung cancer, while fruit intake, physical exercise, and tea drinking were protective factors. Conclusions: Long-term exposure to PM10, PM2.5, and O3 was found to be significantly associated with increased risk of lung cancer, with the risk being greater for non-smokers and persons exposed to cooking oil fumes.

Association of Particulate Matter from Cooking Oil Fumes with Heart Rate Variability and Oxidative Stress

Many studies have reported various cardiovascular autonomic responses to ambient particulate matter (PM) pollution, but few have reported such responses to occupational PM exposures. Even fewer have demonstrated a relationship between PM pollution and oxidative stress in humans. This panel study evaluates the association between occupational exposure to PM in cooking oil fumes (COFs), and changes in both heart rate variability (HRV) and oxidative stress responses in 54 male Chinese cooks. Linear mixed-effects regression models were adopted to estimate the strength of the association between PM and HRV. Participants’ pre- and post-workshift urine samples were analyzed for 8-hydroxy-2′-deoxyguanosine (8-OHdG) and malondialdehyde (MDA). Exposure to PM in COFs from 15 min to 2 h were associated with a decrease in HRV and an increase in heart rate among cooks. The urinary 8-OHdG levels of cooks were significantly elevated after workshift exposure to COFs. The levels of PM2.5, PM1.0, and particulate benzo(a)pyrene in COFs were all positively correlated with cross-workshift urinary 8-OHdG levels. Furthermore, the levels of benzo(a)pyrene in COFs were positively correlated with cross-workshift urinary MDA levels. The effects of COFs on HRV were independent of cross-workshift urinary 8-OHdG levels. Exposure to COFs leads to disturbed autonomic function and an increased risk of oxidative DNA injury among cooks in Chinese restaurants.

Meta-analysis of associations between cooking oil fumes exposure and lung cancer risk

Lung cancer is one of the most common cancers and cooking oil fumes (COF) are considered as the potential dangerous contributing factors. This study, a meta-analysis was conducted to analyse the correlation between exposure to COF and risk of lung cancer. Literature from 1980 to 2020 were searched and 29 studies were selected for analysis. Results showed that population exposed to COF had significant differences in lung cancer prevalence (P < 0.05). The odds ratio (OR) values of different periods (before 2000, 2000–2010 and 2010–2020) were significantly different. Using ventilation equipment had the OR of 0.54. Liao cuisine, Fujian cuisine, Shanghai cuisine, Jingdong cuisine and Shaanxi cuisine had the ORs (95% confidence interval) of 1.91 (1.62, 2.25), 2.38 (1.80, 3.16), 1.56 (1.29, 1.89), 2.58 (1.63, 4.09) and 1.57 (1.16, 2.11), respectively. These results revealed that exposure to COF could increase the risk of lung cancer, but the risk was gradually reduced with the changes of the times and the use of ventilation equipment. Different cooking methods in different regions caused different risks of lung cancer. The risk of lung cancer caused by COF mainly produced by deep-frying, quick-frying, stir-frying and pan-frying is higher than in other methods.

The Toxicity of Cooking Oil Fumes on Human Bronchial Epithelial Cells Through ROS-Mediated MAPK, NF-κB Signaling Pathways and NLRP3 Inflammasome

Cooking oil fumes (COFs) are main pollutants in kitchen and indoor air, which threaten human health. Exposure to COFs can cause respiratory diseases and impair pulmonary function. To investigate the toxicity of COFs on human bronchial epithelial cells (Beas-2B) and explore the underlying mechanisms, MTT assay was conducted to detect the viability of Beas-2B. Intracellular reactive oxygen species (ROS) levels and nitric oxide (NO) levels were determined with DCFH-DA assay and DAF-FM assay. The expression of genes involved in inflammation were measured with quantitative real-time PCR (qRT-PCR). The phosphorylation and the expression of proteins related to Mitogen-activated protein kinase (MAPK), NF-κB signaling pathways were measured with western blot. Our results revealed that COFs decreased Beas-2B cells viability, increased the ROS levels and NO levels in cells and induced apoptosis in Beas-2B cells. The results of qRT-PCR and western blot showed that the expression of NLRP3, p65, iNOS, IL-1β, and the factors related to oxidative stress and inflammation increased, NF-κB signaling pathway and MAPK signaling pathway were activated. This study provided some useful information to alleviate the toxicity of COFs and revealed the possible mechanism for the damage on respiratory system induced by COFs.