Cigarette smoke-induced dysbiosis: comparative analysis of lung and intestinal microbiomes in COPD mice and patients.

BACKGROUND: The impact of cigarette smoke (CS) on lung diseases and the role of microbiome dysbiosis in chronic obstructive pulmonary disease (COPD) have been previously reported; however, the relationships remain unclear. METHODS: Our research examined the effects of 20-week cigarette smoke (CS) exposure on the lung and intestinal microbiomes in C57BL/6JNarl mice, alongside a comparison with COPD patients' intestinal microbiome data from a public dataset. RESULTS: The study found that CS exposure significantly decreased forced vital capacity (FVC), thickened airway walls, and induced emphysema. Increased lung damage was observed along with higher lung keratinocyte chemoattractant (KC) levels by CS exposure. Lung microbiome analysis revealed a rise in Actinobacteriota, while intestinal microbiome showed significant diversity changes, indicating dysbiosis. Principal coordinate analysis highlighted distinct intestinal microbiome compositions between control and CS-exposed groups. In the intestinal microbiome, notable decreases in Patescibacteria, Campilobacterota, Defferibacterota, Actinobacteriota, and Desulfobacterota were observed. We also identified correlations between lung function and dysbiosis in both lung and intestinal microbiomes. Lung interleukins, interferon-É£, KC, and 8-isoprostane levels were linked to lung microbiome dysbiosis. Notably, dysbiosis patterns in CS-exposed mice were similar to those in COPD patients, particularly of Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 4 patients. This suggests a systemic impact of CS exposure. CONCLUSION: In summary, CS exposure induces significant dysbiosis in lung and intestinal microbiomes, correlating with lung function decline and injury. These results align with changes in COPD patients, underscoring the important role of microbiome in smoke-related lung diseases.

A nationwide case-referent study on elevated risks of adenocarcinoma lung cancer by long-term PM2.5 exposure in Taiwan since 1997.

BACKGROUND: The effects of long-term PM2.5 exposures since 1968 on adenocarcinoma lung cancer (AdLC) were not studied before. METHODS: This case-referent study used nationwide cancer registry data since 1997 and air pollution data since 1968 in Taiwan to estimate risks of 30-year PM2.5 exposures on AdLC. Cases were all AdLC, while references were all non-AdLC. Individuals' 30-year PM2.5 exposures were estimated by PM2.5 levels at their residence for 30 years prior their diagnosis dates. We applied multiple logistic regression analyses to estimate PM2.5 exposures on incidence rate ratios (IRRs) between cases and references, adjusting for sex, age, smoking, cancer stage, and EGFR mutation. RESULTS: Elevation in annual ambient PM2.5 concentrations since 1968 were associated with increase in annual age-adjusted AdLC incidence since 1997. AdLC incidences were higher among females, nonsmokers, the elderly aged above 65, cases of stages IIIB to IV, and EGFR mutation. Study subjects' PM2.5 exposures averaged at 33.7 ± 7.4 µg/m3 with 162 ± 130 high PM2.5 pollution days over 30 years. Multiple logistic models showed an increase in 10 µg/m3 of PM2.5 exposures were significantly associated with 1.044 of IRR between all AdLC and all non-AdLC cases during 2011-2020. Our models also showed that females and nonsmokers and adults less than 65 years had higher IRRs than their respective counterparts. Restricted analyses showed similar effects of PM2.5 exposures on IRRs between stage 0-IIIA and IIIB-IV cases and between EGFR+ and EGFR- cases. CONCLUSIONS: Long-term exposures to PM2.5 over 30 years were associated with elevated risks of AdLC against non-AdLC, regardless of gender, age, smoking status, cancer stage, or EGFR mutation.

Effects of antibiotics and metals on lung and intestinal microbiome dysbiosis after sub-chronic lower-level exposure of air pollution in ageing rats.

We investigated the effects of antibiotics, drugs, and metals on lung and intestinal microbiomes after sub-chronic exposure of low-level air pollution in ageing rats. Male 1.5-year-old Fischer 344 ageing rats were exposed to low-level traffic-related air pollution via whole-body exposure system for 3 months with/without high-efficiency particulate air (HEPA) filtration (gaseous vs. particulate matter with aerodynamic diameter of ≤2.5 µm (PM2.5) pollution). Lung functions, antibiotics, drugs, and metals in lungs were examined and linked to lung and fecal microbiome analyses by high-throughput sequencing analysis of 16 s ribosomal (r)DNA. Rats were exposed to 8.7 µg/m3 PM2.5, 10.1 ppb NO2, 1.6 ppb SO2, and 23.9 ppb O3 in average during the study period. Air pollution exposure decreased forced vital capacity (FVC), peak expiratory flow (PEF), forced expiratory volume in 20 ms (FEV20), and FEF at 25∼75% of FVC (FEF25-75). Air pollution exposure increased antibiotics and drugs (benzotriazole, methamphetamine, methyl-1 H-benzotriazole, ketamine, ampicillin, ciprofloxacin, pentoxifylline, erythromycin, clarithromycin, ceftriaxone, penicillin G, and penicillin V) and altered metals (V, Cr, Cu, Zn, and Ba) levels in lungs. Fusobacteria and Verrucomicrobia at phylum level were increased in lung microbiome by air pollution, whereas increased alpha diversity, Bacteroidetes and Proteobacteria and decreased Firmicutes at phylum level were occurred in intestinal microbiome. Lung function decline was correlated with increasing antibiotics, drugs, and metals in lungs as well as lung and intestinal microbiome dysbiosis. The antibiotics, drugs, and Cr, Co, Ca, and Cu levels in lung were correlated with lung and intestinal microbiome dysbiosis. The lung microbiome was correlated with intestinal microbiome at several phylum and family levels after air pollution exposure. Our results revealed that antibiotics, drugs, and metals in the lung caused lung and intestinal microbiome dysbiosis in ageing rats exposed to air pollution, which may lead to lung function decline.

Characteristics of neonicotinoid and metabolite residues in Taiwanese tea leaves.

BACKGROUND: Neonicotinoids are widely used insecticides, and tea is a popular non-alcoholic beverage in Taiwan. However, the levels of neonicotinoids in Taiwanese tea leaves remain unclear. Therefore, this study aims to understand the characteristics of neonicotinoid and metabolite residues in Taiwanese tea leaves. METHODS: In this study, 12 tea leaf samples were collected in Taiwan and extracted by solid-phase extraction before analysis by liquid chromatography-tandem mass spectrometry. In addition, the levels of neonicotinoids were compared with the maximum residue level standards from other countries. RESULTS: In Taiwanese tea leaves, five neonicotinoids and seven metabolites were detected. Different tea species influenced the levels of neonicotinoids and their metabolites in the present study. Moreover, the levels of neonicotinoids and their metabolites in partially fermented leaves were higher than in completely fermented leaves. In Jin-Xuan tea, the levels of neonicotinoids and their metabolites in most winter-harvested teas were lower than in summer-harvested teas. CONCLUSION: The residue levels of neonicotinoids and their metabolites were detectable in Taiwanese tea leaves. Moreover, different tea species, manufacturing processes, and harvest seasons might influence the levels of these pesticides. Therefore, the government should monitor the use of neonicotinoids. © 2021 Society of Chemical Industry.

Lipidomics of children and adolescents exposed to multiple industrial pollutants.

BACKGROUND: There are limited studies on the lipidomics of children and adolescents exposed to multiple industrial pollutants. OBJECTIVES: In this study, we aimed to investigate lipid profile perturbations in 99 children and adolescents (aged 9-15) who lived in a polluted area surrounding the largest petrochemical complex in Taiwan. Previous studies have reported increased risks of acute and chronic diseases including liver dysfunctions and chronic kidney disease (CKD) in residents living in this area. METHODS: We measured urinary concentrations of 11 metals and metalloids and polycyclic aromatic hydrocarbons (PAHs) metabolite 1-hydroxypyrene (1-OHP) as exposure biomarkers, and urinary oxidative stress biomarkers and serum acylcarnitines as early health effect biomarkers. The association between individual exposure biomarkers and early health effect biomarkers were analyzed using linear regression, while association of combined exposure biomarkers with four oxidative stress biomarkers and acylcarnitines were analyzed using weighted quantile sum (WQS) regression. Lipid profiles were analyzed using an untargeted liquid chromatography mass spectrometry-based technique. "Meet-in-the-middle" approach was applied to identify potential lipid features that linked multiple industrial pollutants exposure with early health effects. RESULTS: We identified 15 potential lipid features that linked elevated multiple industrial pollutants exposure with three increased oxidative stress biomarkers and eight deregulated serum acylcarnitines, including one lysophosphatidylcholines (LPCs), four phosphatidylcholines (PCs), and two sphingomyelins (SMs) that were up-regulated in high exposure group compared to low exposure group, and two LPCs, four PCs, and two phosphatidylinositols (PIs) down-regulated in high exposure group compared to low exposure group. CONCLUSION: Our findings could provide information for understanding the health effects, including early indicators and biological mechanism identification, of children and adolescents exposed to multiple industrial pollutants during critical stages of development.

Relationship between renal function and metal exposure of residents living near the No. 6 Naphtha Cracking Complex: A cross-sectional study.

BACKGROUND/PURPOSE: Heavy metals impair renal function, causing chronic kidney disease (CKD), and the petrochemical industry is one of the major environmental metal emission sources. This study aimed to investigate the relationship between renal function and metal exposure among the Taiwanese residents living near a petrochemical industry site. METHODS: We recruited residents near the No. 6 Naphtha Cracking Complex, and they were categorized into a high-exposure (HE) group (N = 190) in Taisi Village and a low-exposure (LE) group (N = 1184) in other villages of Dacheng Township in Changhua County of Taiwan. The urinary nickel, chromium, and vanadium levels of the study subjects were measured and the levels were standardized by urine creatinine, and the estimated glomerular filtration rates (eGFRs) were calculated to estimate renal function by one-time health data. Linear regression models were applied to illustrate the correlations between the distance to the complex and urinary metal levels and renal function; linear and logistic regression models were applied to evaluate the associations between urinary metal levels and renal function indicators. RESULTS: The study subjects living closer to the petrochemical complex had significantly higher urinary nickel, chromium, and vanadium levels and worse renal function than study subjects living farther away. The urinary nickel and chromium levels of the study subjects were associated with their renal function indicators. When the subject's urinary nickel level increased 1-fold, the eGFR level significantly decreased by 0.820 ml/min/1.73 m2. CONCLUSION: Residents living closer to the petrochemical industry were exposed to higher metal levels and had worse renal function, and the nickel exposure of residents was potentially related to their decline in renal function.

Metabolomics of Children and Adolescents Exposed to Industrial Carcinogenic Pollutants.

Studies on metabolomes of carcinogenic pollutants among children and adolescents are limited. We aim to identify metabolic perturbations in 107 children and adolescents (aged 9-15) exposed to multiple carcinogens in a polluted area surrounding the largest petrochemical complex in Taiwan. We measured urinary concentrations of eight carcinogen exposure biomarkers (heavy metals and polycyclic aromatic hydrocarbons (PAHs) represented by 1-hydroxypyrene), and urinary oxidative stress biomarkers and serum acylcarnitines as biomarkers of early health effects. Serum metabolomics was analyzed using a liquid chromatography mass spectrometry-based method. Pathway analysis and "meet-in-the-middle" approach were applied to identify potential metabolites and biological mechanisms linking carcinogens exposure with early health effects. We found 10 potential metabolites possibly linking increased exposure to IARC group 1 carcinogens (As, Cd, Cr, Ni) and group 2 carcinogens (V, Hg, PAHs) with elevated oxidative stress and deregulated serum acylcarnitines, including inosine monophosphate and adenosine monophosphate (purine metabolism), malic acid and oxoglutaric acid (citrate cycle), carnitine (fatty acid metabolism), and pyroglutamic acid (glutathione metabolism). Purine metabolism was identified as the possible mechanism affected by children and adolescents' exposure to carcinogens. These findings contribute to understanding the health effects of childhood and adolescence exposure to multiple industrial carcinogens during critical periods of development.

Increased cancer incidence of Changhua residents living in Taisi Village north to the No. 6 Naphtha Cracking Complex.

BACKGROUND/PURPOSE: Cancer risks of residents living north to the No. 6 Naphtha Cracking Complex has not been studied before. METHODS: Our study subjects were recruited in 2014-16 from three zones north to the No. 6 Naphtha Cracking Complex, which included 229 participants from the Taisi Village (average 5.5 km from the complex), 1333 participants from the other 14 villages in Dacheng Township (9.2 km), and 372 participants from the Zhutang Township (19.9 km). Their occurrence of cancer in years-post-complex-operation (YPO) was defined by having a new cancer recorded (ICD-9: 140-208) in National Health Insurance Research Database since 1999. Poisson regression was conducted to compare incidence rate ratio among three zones in 10-16 YPO. RESULTS: We found that all-cause cancer incidence of 10-16 YPO (per 1,000 person-years) in Taisi Village (8.44) was higher than that in Dacheng (3.42) and Zhutang (2.72). Taisi residents had significantly higher concentrations of V, Cr, Mn, Ni, Cu, As, Cd, and Tl than Dacheng and Zhutang residents. The all-cause cancer incidence rate ratio between 10-16 and 0-9 YPO was 8.44 for Taisi residents. All-cause cancer incidence rate of Taisi residents was 2.55 times higher than Dacheng residents (95% CI: 1.89-3.45) and 2.43 times higher than Zhutang residents (95% CI: 1.54-3.84) in 10-16 YPO. CONCLUSION: We conclude that all-cause cancer risk was significantly increased for Taisi residents living near the No. 6 Naphtha Cracking Complex for 10-16 years after the complex began operating.

Increased inflammation in rheumatoid arthritis patients living where farm soils contain high levels of copper.

BACKGROUND/PURPOSE: Heavy metal pollution in farm soils is a problem in some parts of Taiwan. Copper can be a factor associated with increased disease activities of rheumatoid arthritis (RA). Thus, the aim of this study was to investigate whether copper pollution in farm soils is associated with worsened RA. METHODS: Clinical parameters from 122 RA patients were collected from a medical center in central Taiwan. Levels of heavy metals in the blood were measured using inductively coupled plasma mass spectrometry. Levels of copper in farm soils were retrieved from a national survey. These data were analyzed to find the factors related to RA disease activities. RESULTS: RA patients living where farm soils contained high levels of copper had increased white blood cell counts, erythrocyte sedimentation rate, and disease activity score 28, compared with patients living where copper levels were low. Among the nine types of heavy metal measured in the study, blood levels of copper and nickel correlated with erythrocyte sedimentation rate. CONCLUSION: Our cross-sectional data suggest a correlation between RA disease activity and the level of copper at township farm soils samples. Further longitudinal studies using more rigorous methodologies are warranted to examine whether this correlation is causal.

Assessment of the levels of urinary 1-hydroxypyrene and air polycyclic aromatic hydrocarbon in PM2.5 for adult exposure to the petrochemical complex emissions.

The relationship between external exposure and internal doses of polycyclic aromatic hydrocarbons (PAHs) has not been established for people living in industrial areas. This study was carried out to estimate the relationship between particle-phase PAH exposure and urinary 1-hydroxypyrene (1-OHP) levels among the adults living near a large petrochemical complex in Mailiao, Taiwan. We measured urinary 1-OHP in 781 residents above 35 years old and PM2.5 PAHs within a 20-km radius downwind from the petrochemical complex. Urinary 1-OHP was analyzed by high performance liquid chromatography, while 16 ambient particle-phase PAHs were measured by gas chromatography mass spectrometry. External exposures to individual PAHs at each study subject's address were estimated by kriging interpolation from air sampling results and regressed against the subjects' urinary 1-OHP levels, adjusting for confounding factors. The study population's urinary 1-OHP levels ranged from 0.001 to 3.005 µmol/mol-creatinine with significantly higher levels for females, grilled food consumers, and residents living close to roads. All 16 particle-phase PAHs were present in the study area with total PAH concentrations ranging from 0.111 to 1.982 ng/m(3). The spatial distribution of 4- and 5-ring PAHs identified high-concentration hotspots close to the complex in Mailiao. The multiple regression models showed that the adults' urinary 1-OHP levels were significantly correlated with 5 out of the 16 PAHs, including benzo[a]anthracene, benzo[k]fluoranthene, fluoranthene, pyrene, and dibenzo[a,h]anthracene; a 0.01 ng/m(3) increase in the concentration of these 5 PAHs at the study subjects' addresses was associated with a 20% elevation in urinary 1-OHP levels (µg/g-creatinine). Emissions from a petrochemical complex can elevate particle-phase PAH concentrations in surrounding areas and increase the urinary 1-OHP levels of adults living nearby.

Exposure-associated DNA methylation among people exposed to multiple industrial pollutants.

BACKGROUND: Current research on the epigenetic repercussions of exposure to a combination of pollutants is limited. This study aims to discern DNA methylation probes associated with exposure to multiple pollutants, serving as early effect markers, and single-nucleotide polymorphisms (SNPs) as surrogate indicators for population susceptibility. The investigation involved the analysis of urine exposure biomarkers for 11 heavy metals (vanadium, arsenic, mercury, cadmium, chromium, nickel, lead, manganese, copper, strontium, thallium), polycyclic aromatic hydrocarbon (PAHs) (1-hydroxypyrene), genome-wide DNA methylation sequencing, and SNPs array on all study participants. The data were integrated with metabolomics information and analyzed both at a community level based on proximity to home addresses relative to the complex and at an individual level based on exposure biomarker concentrations. RESULTS: On a community level, 67 exposure-related CpG probes were identified, while 70 CpG probes were associated with urine arsenic concentration, 2 with mercury, and 46 with vanadium on an individual level. These probes were annotated to genes implicated in cancers and chronic kidney disease. Weighted quantile sum regression analysis revealed that vanadium, mercury, and 1-hydroxypyrene contributed the most to cg08238319 hypomethylation. cg08238319 is annotated to the aryl hydrocarbon receptor repressor (AHRR) gene, and AHRR hypomethylation was correlated with an elevated risk of lung cancer. AHRR was further linked to deregulations in phenylalanine metabolism, alanine, aspartate, and glutamate metabolism, along with heightened oxidative stress. Additionally, three SNPs (rs11085020, rs199442, and rs10947050) corresponding to exposure-related CpG probes exhibited significant interaction effects with multiple heavy metals and PAHs exposure, and have been implicated in cancer progression and respiratory diseases. CONCLUSION: Our findings underscore the pivotal role of AHRR methylation in gene-environment interactions and highlight SNPs that could potentially serve as indicators of population susceptibility in regions exposed to multiple heavy metals and PAHs.

Using pollution roses to assess sulfur dioxide impacts in a township downwind of a petrochemical complex.

This study used pollution roses to assess sulfur dioxide (SO) pollution in a township downwind of a large petrochemical complex based on data collected from a single air quality monitoring station. The pollution roses summarized hourly SO2 concentrations at the Taishi air quality monitoring station, located approximately 7.8-13.0 km south of the No. 6 Naphtha Cracking Complex in Taiwan, according to 36 sectors of wind direction during the preoperational period (1995-1999) and two postoperational periods (2000-2004 and 2005-2009). The 99th percentile of hourly SO2 concentrations 350 degrees downwind from the complex increased from 28.9 ppb in the preoperational period to 86.2-324.2 ppb in the two postoperational periods. Downwind SO2 concentrations were particularly high during 2005-2009 at wind speeds of 6-8 m/sec. Hourly SO2 levels exceeded the US. Environmental Protection Agency (EPA) health-based standard of 75 ppb only in the postoperational periods, with 65 exceedances from 0-10 degrees and 330-350 degrees downwind directions during 2001-2009. This study concluded that pollution roses based on a single monitoring station can be used to investigate source contributions to air pollution surrounding industrial complexes, and that it is useful to combine such directional methods with analyses of how pollution varies between different wind speeds, times of day, and periods of industrial development.

Data on lung and intestinal microbiome after air pollution exposure in ageing rats.

Air pollution has been linked to respiratory diseases, and urban air pollution can be attributed to a number of emission sources. The emitted particles and gases are the primary components of air pollution that enter the lungs during respiration. Particulate matter with an aerodynamic diameter of ≤ 2.5 µm (PM2.5) can deposit deep into the respiratory tract via inhalation and has been proposed as a causative agent for adverse respiratory health. In addition, the lung contains a diverse microbial community (microbiome) that maintains normal homeostasis and is significantly altered in a variety of pulmonary disorders. Air pollution, specifically PM2.5, has previously been shown to significantly alter the composition of the lower airway microbiome, which has been linked to decreased lung function in chronic obstructive pulmonary disease (COPD) patients. Surprisingly, the intestinal microbiome has also been implicated in the modulation of pulmonary inflammatory diseases. Therefore, dysbiosis of the lung and intestinal microbiomes pose significant negative effects on human health. This dataset describes the microbial community profiles of the lungs and intestines of ageing rats exposed to ambient unconcentrated traffic-related air pollution for three months. The whole-body exposure system was equipped with and without high efficiency particulate air (HEPA) filtration (gaseous vs. PM2.5 pollution). The data can provide valuable information on lung and intestinal microbiome changes, including that which was only found after traffic-related air pollution exposure.

Association between ambient air pollution exposure and insomnia among adults in Taipei City.

Ambient air pollution was known to cause central nervous system diseases and depressive symptoms. In this study, we examined the associations between air pollution exposure and the prevalence of insomnia in Taipei City of Taiwan. We applied the health information system of electrical medical records of Taipei City Hospital to collect a total of 5108 study subjects (insomniacs N = 912 and non-insomniacs N = 4196) over 18 years old from the family medicine and internal medicine outpatients of six branches of Taipei City Hospital. These patients were grouped into insomniacs and non-insomniacs following the primary insomnia diagnosis (ICD9:780.52, 780.54, 307.41, 307.42, ICD10: G47.00, G47.01, G47.09, F51.01, F51.09) and the prescription times of anxiolytics and hypnotics. We estimated one-year average concentrations of PM2.5, ozone, and NOx before the first date of insomnia diagnosis and the last date of outpatient visit for insomniacs and non-insomniacs, respectively, by using the data of nearest air quality monitoring stations relative to study subjects' residential addresses. Logistic regression analysis was employed to examine the independent effects of air pollution concentrations on the risk of insomnia. One-year average PM2.5, ozone, and NOx levels for insomniacs was significantly higher than those of non-insomniacs. After adjusting for confounding factors, increase each 1(µg/m3) in one-year average PM2.5 showed a statistically significant association with insomnia (the odds ratio 1.610, 95% CI [1.562,1.660]). As to multi pollutants, one-year average PM2.5 (1.624, [1.570, 1.681] and ozone (1.198, [1.094, 1.311]) exposure showed a significant association with insomnia. Subgroup analysis revealed that the influence of PM2.5 and ozone on insomnia have significant risks in people with major chronic disease. This study demonstrated a positive association between PM2.5 and ozone exposure and the prevalence of hypnotic-treated insomnia. Especially, the people with major chronic diseases were with obvious effect of PM2.5 and ozone on risk of insomnia.

Comparison of the PCB serum levels among mother-child pairs in areas of Eastern Japan and Central Taiwan.

Polychlorinated biphenyls (PCBs) have been prohibited for two decades in Japan and Taiwan. The aim of this study was to compare the PCB congeners in maternal and cord serum between two countries. Our study subjects were 248 and 100 mother-child pairs in Japan and Taiwan. The measured levels of 23 serum PCB congeners between two countries were analyzed using gas chromatography-electron capture negative ionization quadrupole mass spectrometry (GC-NICI-qMS). The statistical comparisons were conducted by Student's t-test and principal component analysis with further stratification by maternal age and parity. The maternal total PCBs levels in Japan (426 ± 244 pg/g wet wt) were significantly higher than those in Taiwan (254 ± 155 pg/g wet wt), and the similar results were found in cord total PCBs levels (97 ± 76 and 58 ± 87 pg/g wet wt). It showed different distributions of PCB congeners between two countries. Whether in maternal or cord serum, the CB138, CB153 and CB180 were the highest detectable congeners whether in Japan or Taiwan. And, the CB66, CB99, CB206 and CB209 were only detected in maternal serum of Taiwan. The women of advanced maternal age had higher levels of PCB congeners, especially in Taiwan, and the primiparous women had higher levels of PCB congeners in two countries. In summary, the PCB congeners in Japan's mother-child pairs were with higher levels and different distributions when compared to those in Taiwan, and the maternal age and parity were important factors associated with the PCB levels.

Air-polluted environmental heavy metal exposure increase lung cancer incidence and mortality: A population-based longitudinal cohort study.

BACKGROUND: An increased risk of lung cancer has been observed due to exposure to certain environmental heavy metals. This study elucidated the role of air-polluted heavy metals in the development of lung cancer. METHODS: A longitudinal cohort study involving the general population was conducted to compare heavy metal content among lung cancer patients. The urine concentrations of heavy metals were measured. Questionnaire surveys were designed to collect exposure-related demographic and lifestyle data of the study subjects. RESULTS: Participants residing near the petrochemical industrial area with higher air Cd concentration had relatively higher urinary concentration of Cd. After adjusting for sociodemographic and behavioral factors, tobacco smoking and air pollution remained as potential sources of Cd exposure. An increased prevalence of lung cancer was observed in the highly polluted zone. The risk of lung cancer incidence increased 1.25-fold for each 1 µg/g-creatinine increase in urine Cd level. Patients with lung cancer had significantly higher urinary Cd concentrations. Lung cancer patients with higher urinary Cd level had significantly poor survival (urine Cd level ≥ 1.58 vs <1.58 µg/g-creatinine; survival, medium, 192.0 vs 342.5 days, p < 0.001). At the longitudinal follow-up, participants with higher urinary Cd level had a higher risk of lung cancer incidence (urine Cd level ≥ 1.58 vs <1.58 µg/g-creatinine: 3.91% v.s. 0.87%, hazard ratio: 4.65, p < 0.001). CONCLUSIONS: Accumulation of Cd could be a risk of lung cancer occurrence. High exposure to Cd may result in poor prognosis in lung cancer patients.

A critical exploration of blood and environmental chromium concentration among oral cancer patients in an oral cancer prevalent area of Taiwan.

The growing incidence of oral cancer (OC) in Taiwan has become a crucial public health concern. In particular, Changhua, a county in central Taiwan, carries persistently high OC incidence rate, with an alarmingly high male/female ratio of OC incidence. Previous epidemiological studies had found that the incidence is spatially correlated with the level of soil content to certain heavy metals in the central Taiwan area. Soil and the human body both intake environmental heavy metals, which can be absorbed through various ways. The soil metal concentration is an index of possible environmental exposure to heavy metal, and the blood metal concentration somewhat reflects the level of the exposure on the human body. Metallic carcinogen is likely to generate free radicals and play a role in many cancers, and many studies had reported that environmental exposure to heavy metals is an important risk factor for developing cancer. Studies on animals showed that chronic intake of chromium (Cr) could induce OC. This study aims to explore the association between the Cr concentration in the farm soil and in the blood of OC patients. We recruited 79 OC patients from Changhua County, with their lifestyle being adjusted in regression analysis. The results showed that the Cr concentration in the blood of OC patients is significantly higher than the background value, and is positively associated with the Cr concentration in the soil surrounding their residence (p-value < 0.023). Because Changhua County is only with moderate prevalence of the known OC habitual risk factors, an environmental factor related to heavy metal Cr exposure is suspected. Future investigations may verify the causal relation between Cr and OC.

Assessment of the hyperlipidemia risk for residents exposed to potential emitted metals in the vicinity of a petrochemical complex.

Hyperlipidemia, which is associated with certain environmental factors, is a risk factor for cardiovascular disease. Heavy metals are important pollutants from industrial emissions. However, the relationship between the exposure to heavy metals and the occurrence of hyperlipidemia is limited. This study aimed to investigate the association between serum metal levels and the risk of hyperlipidemia in adults living near a petrochemical complex. Our study subjects were 959 residents aged above 35 years in 11 townships near the largest petrochemical complex in central Taiwan. The serum levels of chromium, arsenic, and mercury in the study subjects were measured. The basic characteristics of the study subjects were collected via a questionnaire survey, and the levels of blood lipid biomarkers were analyzed by health examination. The definition of hyperlipidemia was defined in the provided guidelines. Adjusted generalized linear and logistic regression models were applied to evaluate the associations between petrochemical-related metal exposure and hyperlipidemia. The study subjects had chromium, arsenic, and mercury serum levels of 3.24±3.45, 3.45±4.66, and 1.24±1.08 (µg/L), respectively, and close proximity of the study subjects to the petrochemical complex was significantly associated with increased serum metal levels. The results showed that the total cholesterol levels were significantly associated with the increased serum chromium, arsenic, and mercury levels. And, the LDL-C levels were significantly associated with the increased serum mercury levels. In addition, the increased serum arsenic and mercury levels of the study subjects were significantly associated with higher odds ratios for abnormal total cholesterol levels and the risk of hyperlipidemia. Residing in close proximity to a petrochemical complex and high arsenic and mercury exposure were associated with elevated blood lipid levels and an increased risk of hyperlipidemia among the residential population in the vicinity of the petrochemical industry.

Genetic polymorphism of As3MT and delayed urinary DMA excretion after organic arsenic intake from oyster ingestion.

Organic arsenic intake from seafood is one of the major arsenic exposure routes among the general population. However, organic arsenic metabolism in the human body is not yet clear. The goal of this study was to explore the effects of genetic polymorphisms of human PNP, As3MT and GSTO1 on organic arsenic metabolism among study subjects after oyster ingestion. During the one-week dietary controlled study, fifty study subjects were provided all their daily meals without seafood, except for two designated amounts of oyster given on the fourth day. First morning voided urine samples were provided by the study subjects for 7 consecutive days and analyzed with HPLC-ICP-MS for As(3+), As(5+), monomethylarsonic acid, and dimethylarsinic acid (DMA). Blood samples were collected later for genetic polymorphisms analysis of PNP, As3MT and GSTO1. Study subjects were categorized into "fast-" (n = 32), "medium-" (n = 13) and "slow-metabolizing" (n = 5) groups based on the number of days after ingestion needed for each subject's urinary DMA level reaching peak. Allele frequencies of single nucleotide polymorphisms (SNP) in intron 6 (G/C, p = 0.024) and in intron 10 (T/C, p = 0.039) of As3MT were significantly associated with the urinary DMA excretion. General estimating equation model analysis indicated that the variants of SNP (G>C) in intron 6 and SNP (T > C) in intron 10 of As3MT were respectively associated with higher or lower urinary DMA level by approximately 9 microg L(-1). As3MT was suggested to be one of the major factors affecting the metabolism of dietary organic arsenic in terms of urinary DMA level.