What is the best Asphalt Mix?
Asphalt mix can cause DNA damage so it needs to be taken seriously. Roofers are more likely than the general population to develop cancer, and occupational exposure to polycyclic aromatic hydrocarbons (PAHs) has been identified as a significant risk factor.
asphalt mix design
The main goal of this study was to determine whether phosphorylated histone H2AX (H2AX) could be used as a short-term biomarker of DNA damage in roofers.
On the same week Monday and Thursday, blood, urine, and dermal wipe samples were collected from 20 roofers who work with hot asphalt before and after 6 hours of work (4 sampling periods). Personal monitors were used to measure PAHs in the gas and particle phases during working hours.
Flow cytometry was used to measure H2AX in peripheral lymphocytes, and an ELISA was used to measure 8-hydroxy-2-deoxyguanosine (8-OHdG) in urine.
General linear mixed models were used to assess the relationships between potential predictors and DNA damage (such as sampling period, exposure levels, and work- and lifestyle factors). ANOVA contrasts were used to investigate differences in the mean levels of DNA damage and biomarker.
None of the DNA damage indicators or urinary biomarkers were associated with exposure measurements. In particle-bound form, benzo(e)pyrene was the most common PAH, while naphthalene was the most common in the gas phase.
On both study days, H2AX and 8-OHdG concentrations were higher post-shift than pre-shift.
Cigarette smoking was associated with urinary 8-OHdG, while urinary creatinine was associated with H2AX. For H2ax and 8-OHdG, the between-subject variance to total variance ratio was 35.3% and 4.8%, respectively.
H2AX has shown promise as a biomarker of DNA damage in occupational epidemiology studies. It is easier to detect in large groups and has less variation within subjects than urinary 8-OHdG.
Future research into the kinetics of H2AX phosphorylation in response to chemical exposures could shed light on how this sensitive biomarker of early DNA damage is both transient and persistent.
Workers all over the world are exposed to potentially carcinogenic chemicals on a daily basis. In occupational epidemiology, determining how these exposures contribute to the development of cancer later in life has proven extremely difficult.
Estimating the exposure-cancer relationship becomes more difficult when other environmental and lifestyle factors are present.
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Another issue is the long time lag between exposure to carcinogens and cancer diagnosis. In occupational studies, estimates of current exposures and their relationship to markers of short-term health effects are frequently used.
These markers include DNA damage measurements, which are thought to be accurate predictors of increased cancer risk because they are early indicators of endogenous genomic instability at the tissue level and can be used to detect precancerous lesions, which aids in prevention efforts.
Roofing workers are more likely to develop leukaemia, as well as lung, bladder, stomach, skin, and buccal cavity cancers. Roofers may be particularly vulnerable to asbestos exposure, polycyclic aromatic hydrocarbons (PAHs), and high rates of cigarette smoking.
Working with hot asphalt is a significant source of PAH exposure for this population, which has been linked to sister chromatid exchanges, DNA adducts, and DNA strand breaks.
Asphalt is made up of hundreds of different chemicals, one of which is benzo(a)pyrene (BaP), a known human carcinogen that can be ingested, inhaled, or come into contact with the skin.
Because many PAHs found in asphalt are common in the environment, it is difficult to distinguish between occupational and environmental (non-occupational) exposures.
Smaller molecular weight PAHs, such as 2-ring naphthalene, are mostly found in the gas phase of the atmosphere, whereas larger molecular weight compounds, like 4-ring pyrene, are mostly found in the particulate phase.
Because of the complexity of the mixtures and the sensitivity of some individual PAHs to environmental or analytical conditions, accurate measurement of individual PAHs in the air has proven difficult.
In many workplaces, including roofing, dermal contact can be a significant source of exposure. Because external PAH exposure measurements have limitations, biological monitoring of PAHs has been used for risk estimation.
High molecular weight PAH exposure studies, on the other hand, face similar difficulties due to low exposure levels, undetectable biomarker levels, difficult analytical methods with low sensitivity, and weak correlations between exposure and biomarker levels.
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Urinary metabolites of more abundant and volatile PAHs, such as naphthalene, have previously been proposed to improve the sensitivity of analytical techniques.
PAH exposure can cause the body to produce more reactive oxygen species (ROS). Increased ROS can oxidatively damage biomolecules such as DNA, proteins, and lipids when the cellular antioxidant defense system is compromised.
Recent research has established a link between a lack of cellular protection against oxidative DNA damage and an increased risk of cancer development.
As a byproduct of DNA repair and oxidative damage, 8-hydroxy-2′-deoxyguanosine (8-OHdG) in urine is a reliable biomarker of general oxidative stress and DNA damage linked to occupational and environmental exposures.
Only a few studies have looked at occupational PAH exposure and the DNA damage that results. Asphalt exposure research primarily focused on highway maintenance workers.
In a previous study, the markers 8-OHdG and 1-OHPyr were found to have a good correlation at the end of the work shift in roofers who work with hot asphalt.
One significant disadvantage of 8-OHdG is that its levels can fluctuate as a result of a variety of individual (metabolic events, lifestyle factors such as smoking and alcohol consumption) and environmental (e.g., UV radiation) factors.
Double-strand DNA breaks have also been linked to PAH exposure; this type of DNA damage can be detected in individual cells using phosphorylated histone H2AX (H2AX).
Radiation exposure, cigarette smoke, particulate matter, and other toxic agents have all been linked to higher levels of cellular H2AX. H2AX is thought to be a sensitive marker of DNA damage and an increased risk of cancer development.
The use of H2AX in population studies has been hampered by time-consuming analytical methods.
Although flow cytometry, Western blotting, and ELISA have all been used to detect H2AX, immunofluorescence microscopy is the most widely used. Microscopy and cytometry have both been shown to be useful in determining H2AX formation.
Image cytometry and Laser Scanning Microscopy (LSC) methods, while more expensive and time-consuming than flow cytometry, have the advantage of being able to count and size H2AX foci.
In large-scale studies, a recent study proposed using blood smears made from a single drop of blood as immunostaining techniques.
The following criteria must be met before a biomarker can be used confidently in epidemiology studies:
- The relationship between the biomarker and the exposure in question;
- The formation, distribution, and elimination of the biomarker in humans;
- Variation of the biomarker between and within study participants;
- Baseline values of the biomarker in the general population;
- The cost and difficulty of analytical techniques. Flow cytometry was used to measure the amount of H2AX in lymphocytes from the peripheral blood of roofers who work with hot asphalt.
The study's primary goal was to compare urinary 8-OHdG to H2AX as a short-term marker of DNA damage in roofers exposed to PAHs.
Asphalt DNA Damage
According to our recent findings, urinary 8-OHdG is a promising biomarker for detecting the early effects of occupational asphalt exposure. We broaden our investigation in this section to include H2AX, a different type of DNA damage indicator.
Despite the fact that H2AX measurements have been used in previous experimental studies with human cell lines, this is the first attempt to link human occupational exposures to elevated levels of H2AX.
This is also the first study to use high-throughput flow cytometry to measure H2AX in workers' peripheral lymphocytes, which opens up the possibility of population-based research.
Our findings back up the theory that hot asphalt causes more double-strand breaks and oxidative DNA damage. This effect was stronger on the first of the week and among nonsmokers.
Both DNA damage markers were significantly predicted in this study by the sampling period, which represented four different time points over the course of one workweek.
Cigarette smoking and urinary creatinine were also found to be significant predictors of urinary 8-OHdG and H2AX. Urine dilution has a significant effect on urinary 8-OHdG levels, according to our findings.
Roofers are frequently exposed to extreme heat and the risk of dehydration during a single workday, making this a serious issue.
Furthermore, we discovered that the proportion of unexplained variance in H2AX that differed between subjects was approximately 35.3%, compared to 4.8% for 8-OHdG in urinalysis. Urine 8-OHdG appears to have a higher percentage of within-subject variation.
Because they reflect different types of DNA damage and are obtained from different biological media, these two measurements cannot be directly compared (8-OHdG is obtained from urine, whereas H2AX is obtained from lymphocytes and measures DNA double-strand breaks).
A low ICC value, on the other hand, indicates poor reproducibility and high within-individual variation in a biomarker.
Other studies discovered significant intra-individual variation in urinary 8-OHdG, including 24-hour urine samples.
Numerous individual factors, such as cigarette smoking, dietary considerations, or diurnal fluctuations, can all have an effect on urinary 8-OHdG levels, contributing to the wide intra-individual variation.
In our study, cigarette smoking did not predict 8-OHdG levels, but other individual factors could have influenced its variation.
Dermal wipes had higher pyrene concentrations after work than before. This was not the case with naphthalene. On Monday, urinary 1-OHPyr levels rose steadily throughout the day, whereas naphthalene metabolite levels rose only slightly.
Because naphthalene is the most common PAH in many environments, biomarkers based on naphthalene may aid in the development of more sensitive assays.
However, our findings in this population suggest that environmental and smoking factors can outweigh the effects of occupational naphthalene exposure.
The findings of this study support our previous findings that dermal contact can be a significant route of exposure and that urinary 1-OHPyr is a promising biomarker of occupational exposures in roofers.
cold asphalt mix
Particularly, urinary 1-OHPyr is a well-established biomarker of occupational exposure to PAHs in the urine. PAH exposure levels were generally lower in this study than in previous reports for asphalt workers.
Although the current study's naphthalene metabolite levels were similar to those found in previous research with roofers, post-shift urinary 1-OHPyr levels were significantly lower.
In post-shift samples taken on Monday, nonsmokers had the highest concentration of urinary 1-OHPyr (333.6 ng/l).
This is similar to the pre-shift levels (213 ng/l) discovered in our previous study, where smokers had the highest average post-shift 1-OHPyr levels of 1002 ng/l. In reality, the levels of urinary 1-OHPyr found in this study are comparable to those found in the general population.
Although urinary biomarkers increased during working hours, no reliable correlations between exposure measures, urinary metabolites, and DNA damage were found, making firm conclusions about the relationship between exposure and biomarkers difficult.
This could be explained by the study period's relatively low occupational exposures. Urinary 8-OHdG levels on Monday morning were consistently 36 times lower than in our previous roofer study.
Smoking is an important factor to consider when researching H2AX. The correlation between H2AX and urinary naphthalene metabolites could be explained by their shared association with cigarette smoking, which occurred on the second study day.
This is supported by the fact that smokers had significantly higher urinary 1- and 2-OHNap levels before the work shift on Thursday than after. It's tempting to restrict future assessments to nonsmokers only.
However, given the high percentage of smokers and the difficulties in enrolling participants, such a restriction in the roofer population would be impractical.
In our opinion, the best strategy is to observe and record smoking habits before including it as a potential confounder in final analyses.
The interpretation of the findings is hampered by some study limitations. The main disadvantages are the low exposure levels observed during the study period and the small number of participants.
Repeated sampling at four different time points, on the other hand, resulted in a larger overall sample size. ANOVA was also used to compare measurements taken before and after the work shift, without taking into account repeated measurements.
mastic asphalt mix design
The conditions in the samples collected before and after work are not identical, nor are they independent.
This was only the first step, and it was addressed by the use of linear mixed models, which tested the specific contrasts of interest. In addition, we are aware that some of our hypothesis tests fail to account for multiple comparisons, which may result in a few false positive associations.
Another limitation is widespread exposure to PAHs and other toxins that damage DNA in the environment.
The most widely accepted biomarker of PAH exposure is 1-OHPyr. Pyrene, on the other hand, can be absorbed through inhalation or dermal contact and exists in both gas and particulate forms.
Naphthalene, on the other hand, is primarily absorbed through inhalation and exists primarily in the gaseous phase.
If non-occupational exposure is common, or if occupational exposure is mostly dermal, urinary 1-OHPyr may be a better biomarker. The utility of naphthalene metabolites may be limited in such cases.
This study's PAH biomarkers are indicative of transient exposures. Urinary 1- & 2-OHNap and 1-OHPyr elimination half-lives are estimated to be 4 h and 13 h, respectively.
The rapid elimination of these biomarkers is not expected to limit our study results because the goal of this study is to link short-term PAH exposures to short-term DNA damage markers.
While UV light (UV), environmental chemicals, and even endogenous DNA damage triggers can cause DNA double strand breaks (DSBs), H2AX is an early response to genotoxic insults. Tobacco smoke, which is a common source of PAHs, is also a powerful inducer of DSBs.
Because there are so many variables that can influence H2AX response, distinguishing between baseline levels in the general population and H2AX kinetics after specific exposures are critical.
Previous research has identified two types of H2AX foci: fast transient foci (associated with rapid repair and disappearing within minutes or hours) and residual foci (which persist for days or months).
hot asphalt mix
Only about 20% of DSBs are repaired during the slower phase, while the vast majority are repaired during the fast phase, which is typically completed within minutes.
The persistent foci may be caused by unrepaired damage or slow repair. H2AX repair kinetics may be influenced by age and age-related diseases such as hypertension and cataracts, as well as gender, hormonal response, ethnicity and race, and lifestyle factors (smoking and alcohol consumption).
Long-term occupational exposures may also play a role in the formation of endogenous DSBs and the persistence of the H2AX response. We wanted to evaluate exposure and DNA damage at four different time points when we designed our study.
This was done based on prior experience because pre-shift biomarker levels were known to rise as the workweek progressed.
Another advantage of maintaining four distinct time points was the discovery that behavioral or individual factors, such as smoking, can influence DNA damage levels during the workweek.
Using a high throughput flow cytometry assay, we investigated the potential utility of H2AX as a marker of DNA damage in PAH-exposed workers. We considered its relationship with exposure data, which we couldn't find for H2AX, as one of the factors in our evaluation.
In this group, 8-OHdG, a common DNA damage indicator found in urine, was also unrelated to exposure levels. The relatively low exposure levels could have influenced our analyses.
We looked at H2AX variation between and within subjects as a secondary criterion. We discovered that urinary 8-OHdG varies more within workers than H2AX.
Our findings also show that low-cost techniques like flow cytometry can detect baseline H2AX levels in this population with high accuracy.
Despite the lack of a link to exposure data, we believe H2AX is a sensitive biomarker of early DNA damage associated with occupational exposures. H2AX is a viable option in epidemiology studies due to its low within-subject variability, simplicity, and high throughput methodology.
More research is needed to comprehend baseline H2AX levels, between- and within-individual variation in various study populations, and the effects of dietary, environmental, and lifestyle factors, as well as developmental and degenerative diseases, on this promising biomarker.
This will also aid in the development of criteria for differentiating transient from persistent H2AX foci.
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