Exploring risk transfer of human brucellosis in the context of livestock agriculture transition: A case study in Shaanxi, China

With the booming of worldwide agriculture intensification, brucellosis, one of the most neglected zoonotic diseases, has become an increasing challenge for global public health. Although the transmission patterns of human brucellosis (HB) have been studied in many regions, the dynamic transfer processes of risk and its driving factors remain poorly understood, especially in the context of agricultural intensification. This study attempted to explore the risk transfer of HB between the exact epidemic areas and the neighboring or distant low-risk areas to explain the impact of livestock agriculture intensification and foodborne infections on the transmission of HB in Shaanxi Province as a case study. We adopted multiple approaches, including test-based methods, model-based methods, and a geographical detector to detect the spatial-temporal dynamic changes of high-risk epidemic areas of HB at the county scale. We also quantitatively estimated how the related factors drove the risk transfer of the disease. Results confirmed the risk transfer pattern of HB with an expansion from north to south in Shaanxi Province and identified two primary transfer routes. In particular, in the traditional epidemic areas of the Shaanbei plateau, the farm agglomeration effect can significantly increase the risk of HB. Meanwhile, retail outlets for milk and dairy products were partially responsible for the foodborne infections of HB in the emerging epidemic areas of Xi'an. This study not only contributed helpful insights to support HB control and prevention in the rapid transition of livestock agriculture but also provided possible directions for further research on foodborne HB infections in urbanized areas

Association between <i>ERCC1</i> rs3212986 and <i>ERCC2</i> rs238406 polymorphisms and BPDE-DNA adducts stratified by age.

<p>Association between <i>ERCC1</i> rs3212986 and <i>ERCC2</i> rs238406 polymorphisms and BPDE-DNA adducts stratified by age.</p

Multiple covariates analysis for BPDE-DNA adduct.

<p><i>β_j</i> partial regression coefficient of multiple linear regression.</p><p><i>β_s</i> standardization partial regression coefficient of multiple linear regression.</p>d<p><i>P</i> value for the partial regression coefficient of all covariates to BPDE-DNA adduct levels using multiple linear regression.</p

DNA damage caused by B[a]P exposure detected by a modified comet assay.

<p><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0060006#pone-0060006-g002" target="_blank">Figure 2</a> shows a typical image to reflect the damage levels caused by BPDE-DNA adducts in a randomly selected sample. BPDE covalently binds to cellular DNA and forms interactive complexes. 50 µmol H₂O₂ was used to induce DNA fragmentation, resulting in long tails after electrophoreses in control lymphocytes (see Fig. 2A. control or non-exposed group). BPDE-DNA adducts will capture the short H₂O₂ induced DNA fragments, and consequently, a shorter tail olive (or tail area) will be found in BPDE-exposed cells compared to non-exposed cells (see Fig. 2B. BPDE-exposed group).</p

<i>ERCC1</i>, <i>ERCC2</i> genotypes and BPDE-DNA adducts levels (, n = 282).

a<p><i>P</i> value was obtained using the LSD test or t-test analysis comparing with reference.</p>b<p><i>P</i> value was obtained using one-way ANVOA.</p

BPDE-DNA adducts levels and characteristics of study population (, n = 282).

a<p><i>P</i> value was obtained using the LSD test or t-test analysis comparing with reference.</p>b<p><i>P</i> value was obtained using one-way ANVOA.</p

Association between <i>ERCC1</i> rs3212986 and <i>ERCC2</i> rs238406 polymorphism and BPDE-DNA adducts stratified by smoking index.

<p>Smoking index 1: never smoking;</p><p>Smoking index = average cigarette numbers/day×years.</p

Chromatograms of blank, DNA, BPDE and DNA+BPDE solutions using HPLC-UV detection.

<p><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0060006#pone-0060006-g001" target="_blank">Figure 1</a> reflects the representive HPLC readouts. We used the Chromatograms to detect BPDE-DNA adducts level. The retention time of 9.38 minute was identified to be BPDE-DNA adducts.</p

Comparison of DNA damage caused by B[a]P in different combined minor alleles of ERCC1 rs3212986 and ERCC2 rs238406.

<p>We selected the participants carrying different ERCC1 rs3212986 and ERCC2 rs238406 genotypes and analyzed their induced DNA damage levels induced by B[a]P using the modified comet assay. The damage levels were evaluated by the tail olive moment ratio, tail area ratio and the combined holistic marking respectively. The relationship between the combined minor alleles of ERCC1 rs3212986 and ERCC2 rs238406 and the effect on the repair efficacy of the DNA damage level caused by B[a]P were evaluated. Interestingly, we found following the increasing copies of the combined minor alleles, a reduced DNA repair capacity had been found in the tail olive moment ratio, tail area ratio and the combined holistic marking. (<i>P</i><0.01).</p