In this two-year longitudinal study, the most prominent finding was that occupational exposure to specific metals was negatively linked to serum adiponectin levels in welding workers. Additionally, among heavy metal exposures by WQS regression analyses, Pb was the most negative contributor to serum adiponectin levels. To the best of our knowledge, this study was the first to examine the impacts of occupational metal exposure on serum adiponectin levels using GEE and WQS regression models.
An earlier study reported occupational and environmental exposure to Pb as a probable risk factor for cardiovascular disease . Recent experimental and epidemiological studies have indicated that heavy metal exposure was considered a risk factor for cardiovascular disease and raised the public health burden [19–21]. These review articles discussed the potential correlation between chronic heavy metal exposure—including exposure to Pb, Cd, mercury (Hg), and arsenic (As)—and cardiovascular disease, although the mechanism through which heavy metals act to elevate cardiovascular risks remains disputed. These nonessential heavy metals were all nonthreshold toxins and could display toxic effects at trace concentrations . A review article by Xu et al. proposed that exposure to increased levels of As, Cd, Pb, and Hg was significantly correlated with MetS or comorbid conditions . Another cross-sectional study analysis derived from the Korea National Health and Nutrition Examination Survey of 1,405 subjects indicated that a higher prevalence of MetS was correlated with increased blood Pb concentrations in Koreans . Additionally, a prospective cohort study that enrolled 2,500 young adults of African descent reported that blood As and Pb were significantly associated with elevated fasting glucose with adjustment for percent body fat . In 2000, a review article that contained cell, animal, and human study results suggested the damaging role of Cd in the organic impairment of glucose metabolism; therefore, it contributed to insulin resistance . Numerous studies have established the adverse impacts of toxic heavy metals as potential biomarkers for developing cardiometabolic illnesses.
However, limited literature has explored the relationship between heavy metals and adiponectin levels, especially in occupational exposure. An animal/mouse model executed by Kawakami et al. revealed that Cd exposure caused abnormal adipocyte differentiation, expansion, and function, which lowered the gene expression levels of adiponectin and might contribute to insulin insensitivity . In 2013, the same study group designed another mouse model with Cd administration, which also indicated that Cd exposure induced abnormally smaller adipocytes and decreased adiponectin levels . Another mouse model by the same author found that in vivo exposure to inorganic Co might exhibit a protective function in obesity-related diseases by increasing the expression of adiponectin . This finding was inconsistent with our study results, which demonstrated that occupational exposure to Co might reduce serum adiponectin levels in welding workers. Apart from the animal studies, a longitudinal study by Wang and his colleagues that enrolled 1,228 midlife women without specific heavy metal exposure illustrated that exposure to Cd was associated with an adverse adiponectin profile . Taken together, exposure to Cd was reported as a negative influencing factor on the expression levels of adiponectin, and based on the few studies available, it might also worsen insulin sensitivity and lead to the development of diabetes. In line with earlier reports, our study results revealed that Cd exposure was correlated with decreased serum adiponectin levels, while Co exposure also demonstrated a negative adiponectin profile.
Our preceding study reported that Fe, Zn, Mn, and Cu were dominant among the welding fumes in a shipyard and that welding workers had higher urinary concentrations of Co, Cu, Ni, Mn, Cd, and Zn . Thus, we selected the eight metals to test for in the postexposure urinary samples of the participants in this survey. Among these heavy metal exposures, Pb had the most negative influence on serum adiponectin levels according to the WQS model. One of the mechanisms was probably related to lipid disturbance in occupational Pb exposure. An earlier cross-sectional study by Ademuyiwa et al. suggested that Pb exposure increased cholesterol synthesis and transport to peripheral tissues among petrol station workers . Additionally, aside from conventional mechanisms, telomere shortening and lipid disturbance were also regarded as unignorable roles in the pathway whereby low-level Pb exposure contributed to cardiovascular disease . Moreover, a cross-sectional study of 986 subjects by Sirivarasai et al. indicated that exposure to low Pb levels correlated with deficiency of the enzyme catalase and oxidative stress, which might lead to high blood pressure . In addition to toxic heavy metals, occupational exposure to some essential metals, such as Co, Ni, Cr, and Mn, also negatively affected serum adiponectin levels in our study. Generally, essential metals are necessary for proper cellular growth and function; otherwise, they play a crucial role as cofactors in various enzymes engaged in metabolism and energy production and respond to oxidative stress. Nevertheless, long-standing overexposure to and deficiencies in trace micronutrients could cause adverse health outcomes. Exposure to Mn, Ni, Cr, and Co has increased because of their use as industrial metals in commercial applications over the last century. A recent study summarized that the main detrimental health impact of Mn, Ni, and Co, to a lesser extent, was on lipid peroxidation arising from oxidative stress . Cr had multiple oxidation states ranging from −2 to + 6, in which the trivalent and hexavalent forms were primarily stable structures. Cr(VI) was connected with toxicity and carcinogenicity, while Cr(III) was essential in trace amounts for protein and lipid metabolism and acted as a cofactor for insulin action . Similar to other metals, Cr(VI)-induced oxidative stress and reactive oxygen species production at high concentrations affected the lipid content and DNA of cells, which resulted in lipid peroxidation and DNA damage, respectively . Taken together, the typical negative health effects of exposure to heavy metals seemed to be lipid peroxidation resulting from oxidative stress, although heavy metals could also disturb metabolic functions in various ways.
Some limitations of this study should be considered. First, all welding workers were asked to use respiratory protective devices at work, but office workers were not compelled to wear masks whey they were in the shipyard. Therefore, some office workers might have contacted metal fumes during their workdays if they walked through the welding sites; this might have increased the exposure levels to heavy metals among the office workers more than we expected. Second, to eliminate sampling bias, we confined the work experience of office workers to those who had not held welding jobs within the past two years. However, some office workers in the shipyard had worked in the welding department when they were younger; therefore, the potential effects of earlier exposures to heavy metals on serum adiponectin levels could not be thoroughly assessed, although we corrected the covariates of job tenures. Next, some heavy metals, such as Cr, had multiple oxidation states, but urinary metals analyzed in this study by ICP–MS could not distinguish the amounts of individual oxidation states. Additionally, the welding aerosol composition varied depending on the specific type of welding process and materials used. Nevertheless, the work content of welding workers in this study could not be set up as a uniform welding process. Last, we did not include individual food intake or record dietary recall as confounding variables in this study. However, almost all workers obtained their lunch from factory-provided meals, which diminished the individual differences in the food consumption of the study subjects.