Where is silica dust and polyvinyl chloride found

However, ICAM-1 can be induced on dermal vascular endothelial cells by silica dust. The association between silica exposure and the development of SSc is still unclear. Future studies may determine whether ELAM-1 and ICAM-1 act as disease mediators and may explore their use as biomarkers to determine the role of silica on vascular pathology in autoimmune diseases.

SLE and environmental exposure Environmental influences eg, infectious agents and chemical compounds may modulate an immune response on the development of SLE. Proposed mechanisms by which environmental exposures may influence SLE include production of autoreactive T cells and autoantibodies, stimulation of proinflammatory and anti-inflammatory cytokines, and targeting of end-organ damage.

There have been numerous developments in lupus research pertaining to occupational silica exposure and autoimmune diseases since The number of epidemiological studies has increased substantially. The role of silica in the development of SLE The biases that may arise in a single study of the association of silica and autoimmune disease may be overcome by using various types of study designs.

The exposure assessment methods are critical. Most patients with SLE being women presents a study challenge in that women are less likely than men to have career exposures to silica in the traditional trade industries that involve dust. One way to determine the sensitivity of an exposure assessment method is to examine the sex-specific frequency of exposure among controls, which should be similar to that in studies in comparable populations.

If the observed frequency of silica exposure is lower than expected, the assessment method probably will be an insensitive indicator of exposure.

Six studies published since have provided data on occupational silica exposure and SLE. Two other studies used various registries as data sources to examine SLE in patients with silicosis. A case-control study in the southeastern United States reported a dose-response association with silica dust exposure consistently seen across sex, racial, and educational subgroups Table 2.

Another consideration in evaluating the role of silica exposure in SLE is the relevant dose required for autoimmune effects.

Evidence in previous studies of silica-related autoimmune disease suggests that exposure intensity may be a more important feature than cumulative life-time exposure levels.

These effects are consistent with the observed pathological features of SLE eg, inflammation, altered apoptosis.

Silica is toxic to macrophages, which can lead to apoptosis and increased exposure to intracellular self-antigens. Solvents, pesticides, and air pollutants: relationship to SLE Two community-based studies examined lupus or lupus symptoms in relation to various forms of pollutants. Kardestuncer and Frumkin, 24 reporting a high prevalence of SLE in a small African American community in Georgia, hypothesized that environmental pollutants from industrial sources contributes to the disease.

These 2 studies provide hypotheses that need to be examined in more focused environmental epidemiological studies using newly developed methods to assess exposure to pollutants. There are few epidemiological studies linking pesticide exposure to SLE. Blood levels of dichlorodiphenyldichloroethylene, the long-lasting breakdown product of the organochlorine pesticide dichlorodiphenyltrichloroethane DDT , and several organophosphate pesticide metabolites were examined in a small case-control study in Arizona.

In , a study explored the effect of lifetime farm and occupational organic dust exposures in patients with a recent diagnosis of SLE compared with controls. Notably, a reduced risk of atopy and allergic asthma had previously been associated with childhood agricultural exposures, especially to animals, lending support to the idea that early-life exposure to farm animals also may protect against the development of SLE.

The observation of an inverse association with SLE for adult farm contact with grains or corn was somewhat unexpected, based on previous literature suggesting that grain dust may be proinflammatory in agricultural workers. Classically, this is accomplished through careful avoidance of sun exposure using sunscreen, wearing long-sleeved clothing and hats and strict avoidance of tanning booths.

UVR exposure can induce and exacerbate skin lesions in patients with some subtypes of cutaneous lupus erythematosus. It may induce apoptosis of keratinocytes, whereas in SLE there is a defective clearance of apoptotic bodies, and it may be seen in overexpression of proinflammatory molecules, such as cytokines and chemokines, inducible nitric oxide synthase, and cellular adhesion molecules. Post-apoptotic debris accumulates in germinal centers, activates complement, and serves as a survival signal for B cells that had stochastically become autoreactive in the process of somatic hypermutation.

In the presence of autoantibodies against apoptotic cells or adaptor molecules, the accumulation of post-apoptotic remnants secondarily necrotic cell—derived material causes immune complex formation and their pathological elimination, maintaining auto-inflammation.

These exposures may have a substantial effect on the changing incidence of autoimmune diseases seen in the modern era. A growing number of voices in the scientific community are suggesting the need for expanded research on the effects of modifiable occupational and environmental exposures on the pathogenesis of SLE, SSc, and other systemic autoimmune diseases.

Given that the origins of the majority of autoimmune diseases remain unclear, better understanding of the exposure-disease relationship and its influence on the progression of the disease process would help create preventive measures and effective public health policies. The use of comparable questionnaires and exposure evaluation methods across studies conducted in various populations would provide opportunities for both qualitative comparisons and more formal compilations of data, such as meta-analyses.

Having larger, combined sample sizes along with harmonized exposure assessment methods also would allow for analyses of gene-environment interactions and better understanding of the role of occupational exposures in SLE. Both measuring exposure intensity and clarifying the timing of exposure are crucial in linking exposure to the disease pathogenesis. In addition, more research needs to be performed on the systemic immunogenic effects of harmful occupation-related substances and the autoimmune-related effects of varying exposure scenarios.

Such research may directly affect the development of effective prevention strategies, because efforts to reduce cumulative exposures may require measures different from those in efforts to reduce short-term, high-intensity exposures. Most of the epidemiological literature consists of exposure-disease relationships that have not been confirmed yet in experimental models. The lack of experimental data, where the effect of a single, specific agent in isolation from other compounds is carefully examined, makes it difficult to generalize the data from these uncontrolled studies.

Improved exposure assessment methods and better coordination between experimental models and epidemiological studies are needed to identify the risks more precisely. References 1. Is occupational organic solvent exposure a risk factor for scleroderma? Arthritis Rheum. Relationship between occupational risk factors and severity markers of systemic sclerosis. J Rheumatol. Predictors of survival in systemic sclerosis scleroderma. Many of the methods of removing, repairing, or altering existing concrete structures have the potential for producing vast quantities of respirable dust.

Since crystalline silica in the form of quartz is a major component of concrete, airborne respirable quartz dust may be produced during construction work involving the disturbance of concrete, thereby producing a silicosis hazard for exposed workers. Silicosis is a debilitating and sometimes fatal lung disease resulting from breathing microscopic particles of crystalline silica. Between and , the National Institute for Occupational Safety and Health NIOSH made visits to construction projects where concrete was being mechanically disturbed in order to obtain data concerning respirable crystalline silica dust exposures.

Allison, A. Google Scholar. Download references. You can also search for this author in PubMed Google Scholar. Reprints and Permissions. Biological reactivity of PVC dust. Nature , — Download citation. Received : 02 June Accepted : 14 July Issue Date : 21 August Anyone you share the following link with will be able to read this content:.

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