A comparative assessment of air pollutants of smog in wagah border and other sites in Lahore, Pakistan

Abstract Smog has become the fifth season of Pakistan especially in Lahore city. Increased level of air pollutants (primary and secondary) are thought to be responsible for the formation of smog in Lahore. Therefore, the current study was carried out for the evaluation of air pollutants (primary and secondary) of smog in Wagah border particularly and other sites (Jail road, Gulburg) Lahore. For this purpose, baseline data on winter smog from March to December on primary and secondary air pollutants and meteorological parameters was collected from Environmental Protection Department and Pakistan Meteorological Department respectively. Devices being used in both departments for analysis of parameters were also studied. Collected data was further statistically analyzed to determine the correlation of parameters with meteorological conditions and was subjected to air quality index. According to results, PM 10 and PM 2.5 were found very high above the NEQS. NOx concentrations were also high above the permissible limits whereas SO2 and O3 were found below the NEQS thus have no roles in smog formation. Air Quality Index (AQI) of pollutants was PM 2.5(86-227), PM 10 (46-332), NOx (26-110), O3 (19-84) and SO2 (10-95). AQI of PM 2.5 remained between moderate to very unhealthy levels. AQI of PM 10 remained between good to hazardous levels. AQI of NOx remained between good to unhealthy for sensitive groups levels. AQI of O3 and SO2 remained between good to moderate levels. Pearson correlation showed that every pollutant has a different relation with different or same parameters in different areas. It is concluded from the present study that particulate matter was much more responsible for smog formation. Although NOx also played role in smog formation. So there is need to reduce sources of particulate matter and NOx specifically in order to reduce smog formation in Lahore.

Resumo Smog tornou-se a quinta estação do Paquistão, especialmente na cidade de Lahore. Acredita-se que o aumento do nível de poluentes atmosféricos (primários e secundários) seja responsável pela formação de poluição atmosférica em Lahore. Portanto, o presente estudo foi realizado para a avaliação dos poluentes atmosféricos (primários e secundários) do smog na fronteira de Wagah em particular e em outros locais (Jail road, Gulburg) Lahore. Para este propósito, os dados de referência sobre a poluição atmosférica de inverno de março a dezembro sobre poluentes atmosféricos primários e secundários e parâmetros meteorológicos foram coletados do Departamento de Proteção Ambiental e do Departamento Meteorológico do Paquistão, respectivamente. Dispositivos sendo usados em ambos os departamentos para análise de parâmetros também foram estudados. Os dados coletados foram posteriormente analisados estatisticamente para determinar a correlação dos parâmetros com as condições meteorológicas e foram submetidos ao índice de qualidade do ar. De acordo com os resultados, PM 10 e PM 2,5 foram encontrados muito acima do NEQS. As concentrações de NOx também estavam muito acima dos limites permitidos, enquanto SO2 e O3 foram encontrados abaixo do NEQS, portanto, não têm papéis na formação de smog. O índice de qualidade do ar (AQI) de poluentes foi PM 2,5 (86-227), PM 10 (46-332), NOx (26-110), O3 (19-84) e SO2 (10-95). O AQI de PM 2,5 permaneceu entre níveis moderados a muito prejudiciais à saúde. O AQI de PM 10 permaneceu entre níveis bons e perigosos. AQI de NOx permaneceu entre bom e não saudável para os níveis de grupos sensíveis. O AQI de O3 e SO2 permaneceu entre níveis bons a moderados. A correlação de Pearson mostrou que cada poluente tem uma relação diferente com parâmetros diferentes ou iguais em áreas diferentes. Conclui-se do presente estudo que o material particulado foi muito mais responsável pela formação de smog. Embora o NOx também tenha desempenhado um papel na formação do smog. Portanto, é necessário reduzir as fontes de partículas e NOx, especificamente para reduzir a formação de smog em Lahore.

A comparative assessment of air pollutants of smog in wagah border and other sites in Lahore, Pakistan / Uma avaliação comparativa de poluentes do ar do smog na fronteira de wagah e outros sites em Lahore, Paquistão

Abstract Smog has become the fifth season of Pakistan especially in Lahore city. Increased level of air pollutants (primary and secondary) are thought to be responsible for the formation of smog in Lahore. Therefore, the current study was carried out for the evaluation of air pollutants (primary and secondary) of smog in Wagah border particularly and other sites (Jail road, Gulburg) Lahore. For this purpose, baseline data on winter smog from March to December on primary and secondary air pollutants and meteorological parameters was collected from Environmental Protection Department and Pakistan Meteorological Department respectively. Devices being used in both departments for analysis of parameters were also studied. Collected data was further statistically analyzed to determine the correlation of parameters with meteorological conditions and was subjected to air quality index. According to results, PM 10 and PM 2.5 were found very high above the NEQS. NOx concentrations were also high above the permissible limits whereas SO2 and O3 were found below the NEQS thus have no roles in smog formation. Air Quality Index (AQI) of pollutants was PM 2.5(86-227), PM 10 (46-332), NOx (26-110), O3 (19-84) and SO2 (10-95). AQI of PM 2.5 remained between moderate to very unhealthy levels. AQI of PM 10 remained between good to hazardous levels. AQI of NOx remained between good to unhealthy for sensitive groups' levels. AQI of O3 and SO2 remained between good to moderate levels. Pearson correlation showed that every pollutant has a different relation with different or same parameters in different areas. It is concluded from the present study that particulate matter was much more responsible for smog formation. Although NOx also played role in smog formation. So there is need to reduce sources of particulate matter and NOx specifically in order to reduce smog formation in Lahore.

Resumo Smog tornou-se a quinta estação do Paquistão, especialmente na cidade de Lahore. Acredita-se que o aumento do nível de poluentes atmosféricos (primários e secundários) seja responsável pela formação de poluição atmosférica em Lahore. Portanto, o presente estudo foi realizado para a avaliação dos poluentes atmosféricos (primários e secundários) do smog na fronteira de Wagah em particular e em outros locais (Jail road, Gulburg) Lahore. Para este propósito, os dados de referência sobre a poluição atmosférica de inverno de março a dezembro sobre poluentes atmosféricos primários e secundários e parâmetros meteorológicos foram coletados do Departamento de Proteção Ambiental e do Departamento Meteorológico do Paquistão, respectivamente. Dispositivos sendo usados ​​em ambos os departamentos para análise de parâmetros também foram estudados. Os dados coletados foram posteriormente analisados ​​estatisticamente para determinar a correlação dos parâmetros com as condições meteorológicas e foram submetidos ao índice de qualidade do ar. De acordo com os resultados, PM 10 e PM 2,5 foram encontrados muito acima do NEQS. As concentrações de NOx também estavam muito acima dos limites permitidos, enquanto SO2 e O3 foram encontrados abaixo do NEQS, portanto, não têm papéis na formação de smog. O índice de qualidade do ar (AQI) de poluentes foi PM 2,5 (86-227), PM 10 (46-332), NOx (26-110), O3 (19-84) e SO2 (10-95). O AQI de PM 2,5 permaneceu entre níveis moderados a muito prejudiciais à saúde. O AQI de PM 10 permaneceu entre níveis bons e perigosos. AQI de NOx permaneceu entre bom e não saudável para os níveis de grupos sensíveis. O AQI de O3 e SO2 permaneceu entre níveis bons a moderados. A correlação de Pearson mostrou que cada poluente tem uma relação diferente com parâmetros diferentes ou iguais em áreas diferentes. Conclui-se do presente estudo que o material particulado foi muito mais responsável pela formação de smog. Embora o NOx também tenha desempenhado um papel na formação do smog. Portanto, é necessário reduzir as fontes de partículas e NOx, especificamente para reduzir a formação de smog em Lahore.

A comparative assessment of air pollutants of smog in wagah border and other sites in Lahore, Pakistan.

Smog has become the fifth season of Pakistan especially in Lahore city. Increased level of air pollutants (primary and secondary) are thought to be responsible for the formation of smog in Lahore. Therefore, the current study was carried out for the evaluation of air pollutants (primary and secondary) of smog in Wagah border particularly and other sites (Jail road, Gulburg) Lahore. For this purpose, baseline data on winter smog from March to December on primary and secondary air pollutants and meteorological parameters was collected from Environmental Protection Department and Pakistan Meteorological Department respectively. Devices being used in both departments for analysis of parameters were also studied. Collected data was further statistically analyzed to determine the correlation of parameters with meteorological conditions and was subjected to air quality index. According to results, PM 10 and PM 2.5 were found very high above the NEQS. NOx concentrations were also high above the permissible limits whereas SO2 and O3 were found below the NEQS thus have no roles in smog formation. Air Quality Index (AQI) of pollutants was PM 2.5(86-227), PM 10 (46-332), NOx (26-110), O3 (19-84) and SO2 (10-95). AQI of PM 2.5 remained between moderate to very unhealthy levels. AQI of PM 10 remained between good to hazardous levels. AQI of NOx remained between good to unhealthy for sensitive groups' levels. AQI of O3 and SO2 remained between good to moderate levels. Pearson correlation showed that every pollutant has a different relation with different or same parameters in different areas. It is concluded from the present study that particulate matter was much more responsible for smog formation. Although NOx also played role in smog formation. So there is need to reduce sources of particulate matter and NOx specifically in order to reduce smog formation in Lahore.

Histological heterogeneity in a large clinical cohort of juvenile idiopathic inflammatory myopathy: analysis by myositis autoantibody and pathological features.

AIM: Juvenile idiopathic inflammatory myopathies have been recently reclassified into clinico-serological subgroups. Myopathological correlates of the subgroups are incompletely understood. METHODS: We studied muscle biopsies from 101 children with clinically and serologically defined juvenile idiopathic inflammatory myopathies from the UK JDM Cohort and Biomarker Study by applying the international JDM score tool, myopathological review and C5b-9 complement analysis. RESULTS: Autoantibody data were available for 90/101 cases with 18/90 cases positive for anti-TIF1γ, 15/90 anti-NXP2, 11/90 anti-MDA5, 5/90 anti-Mi2 and 6/90 anti-PmScl. JDM biopsy severity scores were consistently low in the anti-MDA5 group, high in the anti-Mi2 group, and widely distributed in the other groups. Biopsies were classified histologically as perifascicular atrophy (22/101), macrophage-rich necrosis (6/101), scattered necrosis (2/101), clustered necrosis (2/101), inflammatory fibre invasion (2/101), chronic myopathic change (1/101), diffuse endomysial macrophage infiltrates (40/101) and minimal change (24/101). MDA5 cases segregated with the minimal change group and showed no capillary C5b-9-deposition. The Mi2 group displayed high severity scores and a tendency towards sarcolemmal complement deposition. NXP2 and TIF1γ groups showed a variety of pathologies with a high proportion of diffuse endomysial macrophage infiltrates and a high proportion of capillary C5b-9 deposition. CONCLUSION: We have shown that juvenile idiopathic inflammatory myopathies have a spectrum of histopathological phenotypes and show distinct complement attack complex deposition patterns. Both correlate in some cases with the serological subtypes. Most cases do not show typical histological features associated with dermatomyositis (e.g. perifascicular atrophy). In contrast, more than half show relatively mild histopathological changes.

Expression of myxovirus-resistance protein A: a possible marker of muscle disease activity and autoantibody specificities in juvenile dermatomyositis.

AIMS: To evaluate the relationship between expression of myxovirus-resistance protein A (MxA) protein on muscle biopsies by immunohistochemistry and disease activity in juvenile dermatomyositis (JDM) patients. Also, another aim was to investigate whether the expression of MxA is related with myositis-specific autoantibodies (MSA) status in JDM patients. METHODS: 103 patients (median aged 6.3, interquartile range 0.5-15.9) enrolled in the Juvenile Dermatomyositis Cohort and Biomarker Study (JDCBS). Muscle biopsies were stained with MxA and scored. Clinical data at initial presentation were collected and autoantibodies were analysed. Multiple linear regression analysis was performed to estimate the association between MxA expression on muscle fibres and muscle disease activity, and MSA status. RESULTS: Expression of MxA protein on JDM samples was identified in 61.2%. There was a significant association between MxA scores and Childhood Myositis Assessment Scale (CMAS) (P = 0.002), and Manual Muscle Testing of Eight Muscles (MMT8) (P = 0.026). CMAS and MMT8 scores were significantly lower in the group of patients with strong MxA expression. MxA scores differed according to MSA subgroups (P = 0.002). Patients with positive nuclear matrix protein 2 autoantibodies had strong MxA expression, whereas anti-melanoma differentiation-associated gene 5 positive patients had no or weak MxA expression. CONCLUSIONS: This study reveals the significant association between level of MxA expression on muscle fibres and clinical measures of muscular disease activity in JDM patients and MSA status. This confirms type I interferonopathies in muscle fibres of JDM patients which could help with improving treatment outcome in JDM patients and underscoring the distinct pathophysiological pathways in different MSA status.

Effective induction therapy for anti-SRP associated myositis in childhood: A small case series and review of the literature.

BACKGROUND: Anti-Signal Recognition Particle associated myopathy is a clinically and histopathologically distinct subgroup of Juvenile Idiopathic Inflammatory Myositis, which is under-recognised in children and fails to respond to conventional first line therapies. We present three cases where remission was successfully induced using combination therapy with intensive rehabilitation. CASE PRESENTATIONS: Three new patients are reported. All 3 cases presented with profound, rapid-onset, proximal myopathy and markedly raised CK, but no rash. Histology revealed a destructive myopathy characterized by scattered atrophic and necrotic fibres with little or no inflammatory infiltrate. All 3 patients responded to induction with cyclophosphamide, IVIG and rituximab, in conjunction with intensive physiotherapy and methotrexate as the maintenance agent. Our patients regained near-normal strength (MMT > 70/80), in contrast with the current literature where >50% of cases reported severe residual weakness. A literature search on paediatric anti-SRP myositis was performed to June 2016; PubMed was screened using a combination of the following terms: signal recognition particle, autoantibodies, antibodies, myositis, muscular diseases, skeletal muscle, childhood, paediatric, juvenile. Articles in a foreign language were excluded. Nine case studies were found. CONCLUSION: This paper supports the hypothesis that anti-SRP myositis is distinct from other JIIM. It is an important differential to JDM and should be considered where there is severe weakness without rash or if highly elevated muscle enzymes (CK > 10,000 U/l) are found. Early identification is essential to initiate aggressive medical and physical therapy. Greater international collaboration and long-term follow-up data is needed to establish the most effective treatment strategy for this rare group of patients.

Mechanisms of melatonin inhibition of neurohypophysial hormone release from the rat hypothalamus in vitro.

Although melatonin has been reported to influence neurohypophysial hormone release, no binding has been demonstrated in the neurohypophysial system, suggesting melatonin could affect afferent inputs. The effect of neurotransmitter receptor antagonists on the inhibitory effect of melatonin on neurohypophysial hormone release from the rat hypothalamus in vitro was therefore determined. The agents employed were atropine, a muscarinic cholinergic antagonist; mecamylamine, a nicotinic cholinergic antagonist; atenolol, a beta-adrenergic antagonist; phentolamine, a nonselective alpha-adrenergic antagonist; prazosin, a selective alpha-adrenergic antagonist; haloperidol, a dopaminergic antagonist; naloxone, an opioid antagonist; and ibuprofen, a cyclooxygenase inhibitor. Rat hypothalami were incubated in either medium alone or medium containing melatonin or melatonin and antagonist, and hormone release determined. Melatonin (43 nM) significantly inhibited (p < 0.05) vasopressin and oxytocin release. Inhibition was still observed in the presence of atenolol, phentolamine, and naloxone, suggesting that neither adrenergic nor opioid pathways contribute to the response. The inhibitory effect of melatonin on vasopressin and oxytocin release was abolished (p < 0.05) in the presence of atropine (10[-8] M), mecylamine (10[-6] and 10[-4] M), ibuprofen (10[-4] M) and haloperidol (10[-6] and 10[-5] M). The melatonin-induced inhibition of oxytocin release was also attenuated in the presence of prazosin (10[-8] and 10[-6] M). This study suggests that melatonin may influence neurohypophysial hormone release through modulation of afferent pathways mediated by acetylcholine, dopamine, and/or prostaglandin.

Diurnal variation in the effect of melatonin on neurohypophysial hormone release from the rat hypothalamus.

Secretion of neurohypophysial hormones can show a diurnal variation. This has been investigated further in rats maintained on 14 h light:10 h dark using a previously validated in vitro technique employing hypothalami obtained at three different times, 2-3 h after lights on (group A), 13-14 h after lights on (group B), and at 4-5 h after lights off (group C). Hormone release under basal conditions and following stimulation with 40 mM KCl was monitored with or without added melatonin in the concentration range 4.3-43 nM. Basal release of hormone was not influenced by the time of day when the animals were taken, although stimulated release was elevated at midnight. In groups A and B both doses of melatonin significantly reduced basal and stimulated release of vasopressin and basal release of oxytocin (p < 0.01), although no effect was seen in group C animals. Inhibition of stimulated oxytocin release was only produced in group B. These findings suggest that the inhibitory effect of melatonin depends on the time of day and are consistent with the suggestion that melatonin secretion during the dark period may acutely downregulate binding sites in the brain.

Interleukin-1 beta and interleukin-6 stimulate neurohypophysial hormone release in vitro.

Interleukin-1 (IL-1) and interleukin-6 (IL-6) have been reported to stimulate the release of corticotrophin-releasing hormone (CRH) in vitro, the response being antagonized by the cyclo-oxygenase inhibitor, indomethacin. The effects of cytokines on the other major ACTH-releasing hormone, vasopressin (AVP), and the other neurohypophysial hormone, oxytocin, have been little studied, and the published data are conflicting. We have therefore used a previously validated rat hypothalamic explant model to evaluate whether IL-1 beta and IL-6 can directly activate the AVP and oxytocin neurosecretory system. In addition, we have also investigated the effects of inhibition of cyclo-oxygenase (CO) and lipoxygenase (LO) activities on the stimulated release of AVP and oxytocin by means of a series of antagonists, including a specific LO pathway inhibitor. The static rat hypothalamic incubation system used involves fresh hypothalamic explants with consecutive 20-min incubations, and estimation of AVP and oxytocin concentrations in the medium by specific and sensitive radioimmunoassays. It was found that IL-1 beta produced a dose-dependent increase in the release of AVP and oxytocin at doses of 10 and 100 U/ml (P < 0.005). Only at the higher dose of 100 U/ml was IL-6 able to increase significantly AVP and oxytocin release (P < 0.05). These stimulatory effects of IL-1 beta and IL-6 were blocked by cyclo-oxygenase inhibitors, indomethacin (28 microM) and ibuprofen (100 nM), but not by the lipoxygenase inhibitor, BW A4C (10 micrograms/ml), suggesting that prostaglandins are involved in this process.(ABSTRACT TRUNCATED AT 250 WORDS)

Melatonin and its analogs inhibit the basal and stimulated release of hypothalamic vasopressin and oxytocin in vitro.

The secretion of neurohypophyseal hormone and ACTH in the rat has been shown to exhibit circadian rhythms, with high values during the day and low values throughout the night. The neurohypophyseal hormone daily rhythm is altered by exposure to constant light and by pinealectomy. It was, thus, proposed that the observed fall in vasopressin (AVP), oxytocin, and ACTH over the hours of darkness could be related to the release of melatonin seen at this time. Therefore, a study was performed to determine the effect of melatonin on AVP, oxytocin, and CRH-41 release from the isolated rat hypothalamus in vitro. Employing a previously validated technique, rat hypothalami were incubated in either medium alone or medium containing melatonin or one of two melatonin analogs. Hormone release was measured by RIA, and the ratios were calculated and compared by Student's t test, with Dunnett's correction for multiple comparisons. Melatonin showed a dose-dependent inhibition of both basal and stimulated AVP and oxytocin release in the concentration range 4.3 x 10(-10) to 2.5 x 10(-3) M, while having no significant effect on the release of CRH-41. The two melatonin analogs, 2-iodomelatonin and 5-methoxy-N-isobutanoyltryptamine, were also found to inhibit both basal AVP and oxytocin release, indicating that this effect probably depends upon the presence of melatonin receptors in the hypothalamus. This inhibitory modulation of AVP, in the absence of any effect on CRH-41, suggests that melatonin may affect water balance by means of directly inhibiting hypothalamic AVP release. Furthermore, circadian rhythmicity in pituitary-adrenal activity may depend on melatonin modulation of AVP, rather than changes in CRH-41.

Differential effects of neuroexcitatory amino acids on corticotropin-releasing hormone-41 and vasopressin release from rat hypothalamic explants.

We have investigated the direct effects of different neuroexcitatory amino acids (EAA) on the secretion of CRH-41 and arginine vasopressin (AVP) from the rat hypothalamus maintained in vitro. CRH-41 and AVP released in the medium were assayed by RIA before and after incubation with N-methyl-D-aspartate (NMDA), N-methyl-D,L-aspartic acid, kainate (KA), and quisqualate in the concentration range 1 nM to 1 mM in either the absence or the presence of 1 mM Mg2+ in the medium. In the case of NMDA, the effect of the addition of glycine (1 and 10 microM) to the incubation medium was also studied. Finally, we investigated whether different periods of exposure (up to 100 min) of hypothalamic explants to NMDA and KA would affect CRH-41 release. While no EAA was able to induce CRH-41 release under any of the above conditions, 20-min incubations with NMDA in the dose range of 1 nM to 1 mM in the absence of added Mg2+ significantly stimulated AVP release in a dose-related fashion; the maximum effect occurred at a concentration of 1 mM [ratio of stimulated collection/basal collection: NMDA, 1.51 +/- 0.10, controls, 0.86 +/- 0.05 (mean +/- SEM); P < 0.001]. KA also showed a dose-related stimulatory effect in the dose range of 1 nM to 1 mM, with maximal AVP stimulation at 10 microM (KA, 1.91 +/- 0.28; controls, 0.90 +/- 0.03; P < 0.01). The effects of both NMDA and KA on AVP were completely reversed by the competitive antagonists D,L-2-amino-5-phosphonovaleric acid and 6-cyano-7-nitroquinoxaline-2,3 dione, respectively, at doses 10 times higher than those of the agonists. N-Methyl-D,L-aspartic acid stimulated AVP secretion only at a dose of 10 mM (P < 0.01), whereas quisqualate was ineffective at any concentration. The addition of 1 mM Mg2+ to the medium blocked the effect of NMDA, while attenuating AVP stimulation induced by KA. The stimulatory effect of KA on AVP was significantly reduced by D-L-2-amino-5-phosphonovaleric acid (P < 0.05), suggesting that KA may also act through NMDA receptors. Moreover, the presence of glycine in the incubation medium did not result in any effect of NMDA on CRH-41 secretion, nor did it appear to potentiate NMDA-induced AVP release.(ABSTRACT TRUNCATED AT 400 WORDS)