Search

Objectives. The night shift workers were reported to have health consequences, ranging from mild, as cluster headache, to severe, as heart attacks and hormonal irregularities. This study is aimed to perform a systematic review and meta-analyze of the association between the night shift work and the thyroid disorders. Methods. We comprehensively searched eight databases, including PubMed and Google Scholar for the relevant articles. This systematic review and meta-analysis were conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA) statement. Results. We finally included six papers involving 4074 participants. Four papers were eligible for meta-analysis involving 1864 night shift workers and 2017 day shift workers. We against found that thyroid stimulating hormone (TSH) is significantly higher in the night shift group compared to the day shift group. Conclusions. The higher TSH among the night shift workers is attributed to disruption of the circadian rhythm and sleep/wake cycle, with subsequent eating disorders. We proposed that more attention should be paid to the working pattern and the related health consequences.

The interaction between NPs and immune system has been demonstrated, however, the data available are limited. Among all traits, i.s. hydrophilicity, lipophilicity, catalytic activity, composition, electronic structure, capacity to bind or coat surface species and solubility, the dimension, and consequently the surface area, seems to be the main factor that contribute to the interactions of NPs with biological tissues and immune system in particular. Certain NPs accumulate to regional lymph nodes, where they can be taken up and processed by dendritic cells, interact with self-proteins and, hence, modify their antigenicity and elicit altered immune responses and even autoimmunity. Other NPs may induce allergic sensitization, i.e. allergic contact dermatitis to Pd. In vitro studies demonstrated that NPs can modulate cytokine production toward Th1 (Pl, Pd, Ni, Co) or Th2 (Ti, mw and sw Carbon) production patterns. Some NPs have been linked to allergic sensitization, however, It is unlikely that NPs can act as a hapten inducing a specific IgE production, likely they can act as adjuvant and induce a specific pattern of cytokines, antibody and cells that favor allergic sensitization to environmental allergens. Furthermore, NPs demonstrated pro-inflammatory effects in the lung in experimental animal with increased expression on IL-1beta, MIP-1alpha, MCP-1, MIP-2, keratinocyte chemoattractant, TARC, GM-CSF, MIP-1alpha and activation of the stress-activated MAPKs p38 and JNKs. All considered, the available data suggest that through the elicitation of an oxidative stress mechanism, engineered NPs may contribute to pro-inflammatory disease processes in the lung, particularly allergy.

Mast cells are abundant in the heart, among myocardial fibers, around coronary arteries, within arterial intima and intramural vessels, and in atherosclerotic plaques. Their mediators can be released during anaphylaxis and be responsible for acute coronary syndrome. This condition has been described as Kounis syndrome (KS). We report three cases of acute myocardial ischemia, which fulfill the definition for KS. In Cases 1 and 2, the association of intense chest pain with acute urticaria after an allergenic contact (wasp sting and betalactam antibiotic administration, respectively) was suspected to be an attack of angina related to an allergic reaction. No signs of an allergic reaction were observed in Case 3, but only the history of a wasp sting suggested its relationship to loss of consciousness and heart ischemia when hypersensitivity to venom was ascertained. These cases strongly recommend measurement of anaphylactic biomarkers, such as tryptase, during acute coronary syndromes to detect the possible involvement of an allergic reaction. Conversely, measurement of cardiac biomarkers during anaphylaxis, even without obvious signs of myocardial ischemia, might identify patients at risk of myocardial injury.

Zinc (Zn) and selenium (Se) exert regulatory activities on immune functions, while cadmium (Cd) is an immunotoxic agent. The object of this study was to detect effects of 10(-4), 10(-5), and 10(-6) M Cd sulphate, Zn sulphate, and sodium selenite, and their combinations on human peripheral blood mononuclear cell (PBMC) proliferation and IFN-gamma and TNF-alpha production. Only 10(-5) M Zn sulphate significantly enhanced spontaneous PBMC proliferation, which was unaffected by the other salts. At 10(-4) and 10(-5) M, Cd sulphate exerted a dose-response inhibitory action on phytohemagglutinin- (PHA-) stimulated PBMC proliferation and cytokine release, while 10(-4) M and 10(-5) M Zn sulphate and 10(-5) M sodium selenite induced a stimulatory effect on both proliferation and cytokine release; 10(-4) M sodium selenite enhanced only the PBMC proliferation; at 10(-6) M, none of the salts changed the PHA-stimulated immune activity. Moreover, 10(-4) and 10(-5) M Zn and 10(-5) M Se strongly upregulated IFN-gamma (a Th1 cytokine) release, even in presence of 10(-5) M Cd, and reduced the inhibitory effects of Cd on PBMC proliferation and TNF-alpha release. This study confirms that Zn and Se both strongly enhance cytokine release induced by mitogenic stimulation, showing also that Zn acts with a broader range of concentrations than Se. This suggests that dietary excess of Se may not have beneficial effects.

The object of this study is to determine the cytokine release from PBMCs exposed to Pd model nanoparticles emitted from catalytic converters. PBMCs of 8 healthy non-atopic women were incubated in the presence of Pd nanoparticles (5-10 nm) or salt (potassium hexa-chloropalladate) 10-5 and 10-6 M. Release of cytokines in supernatant of PBMCs was then determined. In cultures without LPS, IL-10 and IL-17 release from PBMCs was inhibited by Pd salt, while Pd nanoparticles inhibited TNF-alpha and IL-17 release. In LPS-stimulated cultures, release of IFN-gamma, TNF-alpha, IL-10 and IL-17 was inhibited by Pd salt, whereas IFN-gamma release was enhanced and TNF-alpha and IL-17 release was inhibited by Pd nanoparticles. In conclusion, Pd salt inhibits cytokine release, whereas Pd nanoparticles exert modulatory effects enhancing the release of IFN-gamma, a Th1 cytokine typical of delayed allergic reactions. This result is interesting considering the increase of allergic contact dermatitis to Pd in people exposed to Pd nanoparticles in urban environments.

In vitro immune effects of Pt compounds of occupational and/or environmental importance, or those used in cancer treatment were studied. Spontaneous and PHA-stimulated proliferation of peripheral blood mononuclear cells (PBMC) and in vitro release of TNF-alpha, IFN-gamma, and IL-5 were assessed in presence of high and very low concentrations of Pt salts: 10(-4) and 10(-7) M (NH4)2[PtCl6], (NH4)2[PtCl4], PtCl4, PtCl2, Na2PtI6, and cis-diaminedichloroPt (CisPt). Spontaneous and PHA-stimulated PBMC proliferation were both inhibited by 10(-4) M (NH4)2[PtCl6] and (NH4)2[PtCl4], while only PHA-stimulated proliferation was inhibited by 10(-4) M CisPt, without significant effects of the other Pt salts. TNF-alpha release from PBMC was reduced by 10(-4) M (NH4)2[PtCl6] and INF-gamma release was reduced by 10(-4) and 10(-7) M hexa- and tetrachloroplatinate and 10(-4) M Na2PtI6, but not by other Pt salts. IL-5 release (related to the Th2 immune response) was inhibited by 10(-4) M (NH4)2[PtCl6], (NH4)2[PtCl4] and Na2PtI6, but it was enhanced by both 10(-4) and 10(-7) M PtCl4. PtCl2 did not influence the immune effects. The study shows Pt salts have immune effects and their potency is ranked in the following order: (NH4)2[PtCl6](NH4)2[PtCl4]Na2PtI6 and CisPtPtCl4PtCl2. These results indicate that certain Pt salts affect lymphocyte proliferation and cytokine release. The intracellular mechanisms responsible for such effects have not been identified.

The effects of graded concentrations of Pt, Pd, and Rh salts on spontaneous and PHA-stimulated peripheral blood mononuclear cell (PBMC) proliferation and IFN-gamma, TNF-alpha, and IL-5 release were the focus of this study. Spontaneous PBMC proliferation was inhibited by all 10(-4) M salts (with the exception of PtCl2), while it was enhanced by 10(-5) M PtCl2 as well as by 10(-5) and 10(-6) M (NH4)2[RhCl6] and RhCl3 (but not by 10(-7) M salts). Pt, Pd, and Rh compounds showed similar effects on PHA-stimulated PBMC proliferation and cytokine release; however, the effects on IFN-gamma release were stronger. Thus, 10(-4) and 10(-5) M (NH4)2[PtCl6] and 10(-4) M (NH4)2[PtCl4] inhibited the PHA-stimulated immune activity; 10(-4) M PtCl2 did not exert activity, while 10(-6) M (NH4)2[PtCl6] and 10(-5) and 10(-6) M (NH4)2[PtCl4] and PtCl2 enhanced PBMC proliferation and/or cytokine release. (NH4)2[PdCl6] showed stronger dose-related inhibitory effects (present also at 10(-7) M concentration) on PHA-stimulated proliferation and cytokine release than (NH4)2[PdCl4], PdCl2, or Rh salts; the inhibitory activity of (NH4)2[RhCl6] was slightly higher than that of RhCl3. In conclusion, this study shows that: (a) the immune capacity of Pt, Pd, and Rh depends on speciation; (b) low concentrations of Pt salts stimulate spontaneous and PHA-stimulated immune responses; (c) the in vitro activity of Pd compounds (which are only inhibitory) is higher than that of Pt and Rh salts. These findings are consistent with the observations that sensitization and allergic contact dermatitis in response to Pd are increased in the general population, although the roles of cross-sensitization to Pd and Ni are difficult to determine.

The interaction between NPs and immune system has been demonstrated, however, the data available are limited. Among all traits, i.s. hydrophilicity, lipophilicity, catalytic activity, composition, electronic structure, capacity to bind or coat surface species and solubility, the dimension, and consequently the surface area, seems to be the main factor that contribute to the interactions of NPs with biological tissues and immune system in particular. Certain NPs accumulate to regional lymph nodes, where they can be taken up and processed by dendritic cells, interact with self-proteins and, hence, modify their antigenicity and elicit altered immune responses and even autoimmunity. Other NPs may induce allergic sensitization, i.e. allergic contact dermatitis to Pd. In vitro studies demonstrated that NPs can modulate cytokine production toward Th1 (Pl, Pd, Ni, Co) or Th2 (Ti, mw and sw Carbon) production patterns. Some NPs have been linked to allergic sensitization, however, It is unlikely that NPs can act as a hapten inducing a specific IgE production, likely they can act as adjuvant and induce a specific pattern of cytokines, antibody and cells that favor allergic sensitization to environmental allergens. Furthermore, NPs demonstrated pro-inflammatory effects in the lung in experimental animal with increased expression on IL-1beta, MIP-1alpha, MCP-1, MIP-2, keratinocyte chemoattractant, TARC, GM-CSF, MIP-1alpha and activation of the stress-activated MAPKs p38 and JNKs. All considered, the available data suggest that through the elicitation of an oxidative stress mechanism, engineered NPs may contribute to pro-inflammatory disease processes in the lung, particularly allergy.

The aim of this study is the immune response of the staff of a university and a museum (referent group). 46 women and 40 men with similar mean age (44 years) were investigated. The first group of women (A) worked in libraries, B in offices in contact with students, C as secretaries and D in a museum. One group of men (E) was composed of employees of the university, one worked in a library temporarily located underground (F) and the last group (G) in a museum. STAI I and II (state and trait anxiety, respectively), and occupational stress were measured by questionnaires. Blood samples were collected for determining NK cytotoxic activity vs human erythroleukaemia cells and the lymphocyte subsets CD45+, CD45+-CD3+, CD45+-CD3+-CD4+, CD45+-CD3+-CD8+, CD45+-CD3-CD8+, CD3+-CD16+-56+ and CD3+-CD19+. Group B showed significantly higher score of occupational stress and STAI I (but not of STAI II) than the other groups of women. Group F of men showed higher levels of occupational stress and both STAI I and II than groups E and G. Group B of women and F of men also showed significantly lower values of blood cytotoxic activity. The scores of STAI I and II were negatively correlated with the cytotoxic activity expressed per ml of blood and/or total lymphocytes. and/or NK CD45+-CD16+-CD56+ cells. In conclusion, this study shows that occupational stress may increase anxiety which is negatively correlated with blood cytotoxic activity. This is a useful tool for determining the health effects of stress.

The use of particles from micro to nanoscale provides benefits to diverse scientific fields, but because a large percentage of their atoms lie on the surface, nanomaterials could be highly reactive and pose potential risks to humans. Due to their wide range of application, Cobalt nano-particles are of great interest both in industry and in life-science. To date, there are few studies on Co nano-particle toxicology. In this respect, this study aims at evaluating in vitro the potential interference of Co nano-particles on the production of several cytokines (IL-2, IL-4, IL-6, IL-10, IFNgamma and TNFalpha) by PBMCs, comparing their effects to those of Co micro-particles and Co solution (CoCl2). Cells were cultured in Opticell flasks with escalating concentrations (10-5, 10-6 and 10-7 M), of Co nano and micro-particles and CoCl2 or without metal. Cytokines were quantified in the supernatants using a human Th1/Th2 cytokine cytometric bead array. Co micro-particles showed a greater inhibitory effect compared to other Co forms. Its inhibitory activity was detected at all concentrations and towards all cytokines, whereas Co solutions selectively inhibited IL-2, IL-10 and TNF-alpha at maximal concentration. Co nano-particles induced an increase of TNF-alpha and IFN-gamma release and an inhibition of IL-10 and IL-2: a cytokine pattern similar to that detected in the experimental and clinical autoimmunity. On the basis of the obtained data, immune endpoints should be sought in the next series of studies both in vitro and in vivo in subjects exposed to cobalt nano-particles.