Combined exposure to PM2.5 and PM10 in reductions of physiological development among preterm birth: a retrospective study from 2014 to 2017 in China.

Background: Preterm birth (PTB) has been linked with ambient particulate matter (PM) exposure. However, data are limited between physiological development of PTB and PM exposure. Methods: Trimester and season-specific PM exposure including PM2.5 and PM10 was collected from Jiaxing between January 2014 and December 2017. Information about parents and 3,054 PTB (gestational age < 37 weeks) outcomes such as weight (g), head circumference (cm), chest circumference (cm), height (cm) and Apgar 5 score were obtained from birth records. We used generalized linear models to assess the relationship between PTB physiological developmental indices and PM2.5, PM10 and their combined exposures. A binary logistic regression model was performed to assess the association between exposures and low birth weight (LBW, < 2,500 g). Results: Results showed that there were 75.5% of low birth weight (LBW) infants in PTB. Decreased PM2.5 and PM10 levels were found in Jiaxing from 2014 to 2017, with a higher PM10 level than PM2.5 each year. During the entire pregnancy, the highest median concentration of PM2.5 and PM10 was in winter (61.65 ± 0.24 vs. 91.65 ± 0.29 µg/m3) followed by autumn, spring and summer, with statistical differences in trimester-specific stages. After adjusting for several potential factors, we found a 10 µg/m3 increase in joint exposure of PM2.5 and PM10 during the entire pregnancy associated with reduced 0.02 week (95%CI: -0.05, -0.01) in gestational age, 7.9 g (95%CI: -13.71, -2.28) in birth weight, 0.8 cm in height (95%CI: -0.16, -0.02), 0.05 cm (95%CI: -0.08, - 0.01) in head circumference, and 0.3 (95%CI: -0.04, -0.02) in Apgar 5 score, except for the chest circumference. Trimester-specific exposure of PM2.5 and PM10 sometimes showed an opposite effect on Additionally, PM2.5 (OR = 1.37, 95%CI: 1.11, 1.68) was correlated with LBW. Conclusion: Findings in this study suggest a combined impact of fine particulate matter exposure on neonatal development, which adds to the current understanding of PTB risk and health.

Immunization of nonautoimmune mice with DNA binding domains of the largest subunit of RNA polymerase I results in production of anti-dsDNA and anti-Sm/RNP antibodies.

Antibodies against the N-terminal (NT) but not the basic domain (BD), DNA binding regions of the largest subunit (S1) of RNA polymerase I (RNAPI) were detected in the sera of MRL-lpr/lpr lupus mice. Antibodies against both RNAPI(S1)-NT and -BD, as well as other systemic lupus erythematosus (SLE) autoantigens (La, ribosomal P proteins and Sm/RNP) were produced by rabbits immunized with anti-DNA antibodies that had been affinity purified from SLE patients. Immunization of nonautoimmune mice (Balb/c) with RNAPI(S1)-NT, RNAPI(S1)-BD, or La in the form of GST fusion proteins, induced production of anti-double-stranded (ds) DNA and anti-Sm/RNP. GST-P1 did not induce an anti-dsDNA response in these mice. These results demonstrate that RNAPI(S1)-NT, RNAPI(S1)-BD and La can participate in an anti-autoantigen/anti-DNA antibody loop during an SLE-like autoimmune response.

Autoantibodies and autoantigens in the urine of SLE patients.

Autoantibodies against RNA polymerase I (RNAPI), DNA, La and ribosomal P proteins were detected in the urine of systemic lupus erythematosus (SLE) patients, many with normal protein excretion rates. In a number of cases, the antibodies were detectable in the urine but not the serum sample of the same patient. The presence and relative concentrations of the urinary autoantibodies correlated with disease activity. RNAPI antigens were detected in the urine of SLE patients by radioimmunoassay and immunoblotting using rabbit antisera prepared against the purified holoenzyme. Immunoaffinity purification of the rabbit anti-RNAPI with SLE urine proteins resulted in antibodies directed primarily against the largest RNAPI subunit (S1; 194 kDa). Antibodies prepared against recombinant fusion proteins representing the DNA binding regions of human RNAPI(S1) reacted with a 35 kDa SLE urinary protein, a putative fragment of RNAPI(S1). Ribosomal protein P0 was detected in SLE patients' urine by immunoblotting, using rabbit antiserum prepared against recombinant human P1 fusion protein. The relative quantities of urinary P0 correlated with disease status. Analysis of urinary autoantibodies and corresponding antigens in conjunction with analysis of serum autoantibodies may be of value for the purpose of monitoring disease activity.